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Resilience-based Development Response to the crisis in Syria and neighbouring Countries
Five years into the conflict in Syria, over 50 percent of the population is either internally displaced or has fled the country. The fighting has drastically rolled back the region's human development achievements from 113 out of 189 in 2010 before the conflict to 173 out of 183 countries by the end of 2014.
Over 200,000 people have been killed and nearly 12 million Syrians are displaced (includes refugees and internally displaced persons). Infrastructures and economic sectors have been devastated due to prolonged conflict. Syria has incurred a cumulative economic loss of US$203 billion by the end of 2014, a loss four times its GDP in constant prices in 2010. 54.3% of the Syrian labor force is unemployed (3.339 million people). As a result, over 11 million dependents who relied on primary breadwinners have been affected. 75 percent of the population living in poverty. At the same time, millions of Syrians continue seek refuge in neighboring countries, already vulnerable host communities are struggling with the influx of new refugees.
- 75 percent of Syrians now living in poverty. Of this 55 percent are unable to access basic food and non-food items for survival. 20 percent living in active conflict zones face abject poverty and are facing starvation and malnutrition.
- Nearly 3.8 million registered refugees in Egypt, Iraq, Jordan, Lebanon, Turkey and North Africa as of March 15 2015.
- Over 220,000 killed in fighting, with over 800,000 injured, and 12.2 million now need humanitarian assistance.
- Refugees will soon make up one-third of the population in Lebanon and camp Za'atri in Jordan, which hosts nearly 84,000 Syrian refugees, is the second-largest refugee camp in the world. The Syria Crisis the largest political, humanitarian, and development challenge of our times.
- 97% of 225,000 Syrian refugees in Iraq are in Kurdistan which also hosts many of the 2.1 million Iraqi Internally Displaced Persons who have fled their homes in Iraq due to ongoing conflicts stemming from the Syria Regional Crisis.
In host countries, insufficient services such as health, education, sanitation, housing and socio-economic infrastructure, coupled with a collapse in economic opportunity and increased competition for jobs, are exacerbating deprivation. Rising tensions have begun to threaten social cohesion and the rule of law.
As one of development agencies in Syria with the largest presence, UNDP works with affected communities to help them cope, rebuild, recover and protect development gains, for example by providing temporary jobs to affected people, clearing debris and helping local businesses to recover productive assets, supporting basic health services such as ambulatory service, reproductive health support, assistance for people with disabilities, creating solid waste removal projects and other initiatives to prevent communicable and diseases which emerge when communities face poor nutrition, low healthcare support, and poor living conditions.
In countries neighboring Syria, UNDP supports host communities to cope with the influx of refugees by improving infrastructure, and boosting local economic and employment opportunities, especially for vulnerable groups, such as young people, those with disabilities and women - while helping to resolve, mediate and prevent conflict.
UNDP's development approach focuses on building resilience and ensuring that communities not only recover from the crisis but also improve the longer-term development prospects needed to move towards a lasting peace.
Projects and Initiatives
News on Syria
$4.5 million support towards Host communities and Refugees from Syria in Lebanon
The United Nations Office for the Coordination of Humanitarian Affairs (OCHA) in Beirut announced the donation of around $4.5 million from its Emergency Response Fund (ERF)more
Providing sustainable livelihood opportunities to vulnerable youth amongst the Syrian refugees and hosting communities in Dohuk and Erbil
The continuing unrest and instability in Syria is increasingly impacting the internal situation of Iraq, and particularly of the Kurdistan Region which in May 2014 ismore
Flood risk management structures in Aarsal and Ras Baalbek save lives of the locals and the Syrian refugees in Bekaa region
"The damage that we used to witness before did not happen this time" wrote the Mayor of Aarsal to UNDP on the 12th of May 2014more
UNDP and the UK boost Cooperation in Supporting of the Health Care Center in Bekaa Area
"Despite the poverty we are living in, the center has helped me and my kids a lot especially that getting medical care in Lebanon is toomore


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Seeing the world and protecting the environment don't exactly go hand in hand. The farther from home you travel, the more fuel and energy you burn and the greater the carbon footprint is that you leave behind.
Because they emit less carbon dioxide per passenger, train and bus travel is generally seen as being more environmentally friendly than flying or driving. But trains and buses don't go everywhere you need to – or as fast as you need them to – and sometimes that cross-country or international flight is your only option.
Concerned about air pollution from flying? Some airline companies offer carbon offsets. Photo By Martynr/Courtesy Flickr
Don't be disheartened. Traveling by plane doesn't mean you can't help the environment. If you can't reduce your pollution, at least you can make up for it.
Although there's no way to reduce your plane's carbon emissions, some airlines and travel companies offer offsets, or donations to projects that produce energy without burning fossil fuels or emitting greenhouse gases. In other words, the donation to the project is supposed to "offset" the greenhouse gases the plane will emit. The best part? It doesn't cost that much.
Expedia offers its customers the opportunity to buy carbon offsets through TerraPass, which funds wind farms, landfill gas capture and farm power. A round-trip flight of up to 2,200 miles costs travelers only $5.99 to offset 1,000 pounds of CO2. A cross country flight of 6,500 costs $16.99, and offsets for an international flight (up to 13,000 miles) cost $29.99.
Expedia isn't the only company partnering up for a greener globe. Orbitz offers its travelers offsets through Carbonfund.org. Offsets for a 6,000-mile trip through Carbonfund.org costs about $11.50, and offsets for an international flight of 20,000 miles costs about $38.
Is this just a way to make amends for feeling guilty about flying? Maybe. But if you can't avoid flying, buying offsets certainly can't hurt.
What do you think about carbon offsets? Have you or would you ever purchase them, and why? Leave a comment to discuss.

subset: commoncrawl


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In part 1, I relayed a story of the common carp. Long ago, the carp was domesticated by monks to have fewer, patchy scales, making the fish easier to prepare and eat.
I thought that I was doing my best to stay on top of evolution-related news, but now I fear that I've grown lazy, and for that I blame Ed Yong. Yong is a tremendously talented writer who, I can only assume based on his output, has somehow genetically engineered himself to require no sleep. We highlight his work every week in What We're Reading posts, and I have come to rely on him to tell me what's happening in the world of evolution research.
The New York Times published eight essays as part of its "Week of Misconceptions" series in early April.
Yes, it's true—we're coming to the end of our month of trees here at Misconception Monday. This week brings three more misconceptions to tackle, including the one that needles me the most as a paleontologist. I'm saving that one for last.
This week I am cutting to the chase! No long jargon-laden intros, no musings about jargon—now it's all about the trees, baby! In fact, it's all misconceptions about trees, and we're going to tackle three of them.
Last week I offered a long introduction to evolutionary trees, and I apologize that it was so long that we didn't even get to the misconceptions. But as you realized, some common vocabulary is required if we're going to make sense of evolutionary trees, and I felt that it was worth the time to get it all straight—even if we don't all 100% agree on 100% of the terms (I'm looking at you, John Harshman!). This week, I again delay a bit to talk about the role of jargon in communication, but good news! I do manage to eek in our first tree misconception.
Credit: UCMP Understanding Evolution (http://evolution.berkeley.edu)
Evolutionary trees are everywhere—in textbooks, museums, trade books, and journals and magazines—and they are key to understanding common descent. And yet, to interpret them properly, you need to understand some specialized vocabulary and to adopt a specific mindset. Basically: It's tough to talk tree.
In Part 1, I told you about my work with the 1918 influenza virus, and promised to tell you more about why the Highly Pathogenic Avian Influenza H5N2 (HPAIH5) influenza strain that is currently rampaging through chicken farms in the Midwest is unlikely to jump to humans.
Back in the day, whenOutdoor flu ward, 1918, Walter Reed Hospital
I was the kind of scientist who worked in a lab, I spent seven years deciphering the genetic sequence of the 1918 influenza virus at the Armed Forces Institute of Pathology (AFIP) in Washington D.C. The pandemic caused by this virus, which erupted in three distinct waves beginning in the late summer of 1918 and ending in the spring of 1919, killed somewhere between 20 and 50 million people worldwide. Never before or since has an influenza virus killed so many, nor returned in so many waves so quickly. Could it happen again? Could the outbreaks of avian influenza (subtype H5N2) currently devastating chicken farms in the Midwest lead to 1918-scale disaster?
"Greenhouse gases" and "the greenhouse effect" are terms used to describe some of the most basic concepts related to global warming. If students learn anything about climate change, they usually learn about these first. This is good in some ways, because these are the fundamental concepts in scientific explanations of how climate change works and why the earth is warming. But the specific metaphor here, comparing the Earth to a greenhouse with carbon dioxide and water vapor cast in the roles of panes of glass, has been criticized on the grounds that it may engender a misunderstanding of the science.
National Center for Science Education, Inc.
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3rd Annual Strong Bones Gala: Chicago
The 3rd Annual Strong Bones Gala Chicago
will be on September 30, 2017 at the Chicago Cultural Center.
Ticket Categories:
Single $100 - admission for one to enjoy open bar, all you care to eat and auctions
Couple $180 - admission for a couple to enjoy open bar, all you care to eat and auctions
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If you would like to coordinate a table of ten but have each person pay individually, answer "yes" when asked if you are "part of a table" and enter the name of your party coordinator in the field provided.
We can't wait to see you on September 30th!
Thank You to our Sponsors
Saturday, September 30, 2017


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Use your f-pawn
We have recently added two new chess training videos, both featuring openings where White makes early use of the f-pawn. These openings are slightly unusual but have at http://tadalafilonline-best4ed.com/ least two advantages for the casual players. cialis as a bph treatment First, you'll be more familiar with the positions than your opponents and have a good chance to outplay them. Second, a mistake generic cialis in defense can quickly lead to a winning attack for viagra pills White.
In the first video International Master Andrew Martin advocates playing the Grand Prix Attack against the Sicilian Defense. This puts pressure on Black from the phone tracker by satellite outset and contains a lot cialis viagra of poison – a vicious king-side attack often defeats Black. sildenafil
A great benefit is that this cialis in generic is an easy-to-learn opening which avoids memorizing a lot of moves to counter the Sicilian Defense. custom essay writing There is side effects viagra also something buy generic viagra online for Black players – a good clomid http://buyessayeasy365.com/ defensive system is shown against the "premature" 2.f4. For users who want even more there cheap generic cell phone tracker tadalafil uk sildenafil dosage is also the Foxy video on The f4 Sicilian by Grandmaster James Plaskett.
Next International Master Andrew Martin presents coverage on the unusual Bird's Opening, which starts with 1.f4. This will appeal to original players who like positions with little theory from where they sildenafil oral can outplay their opponent.
Arguably the openings greatest exponent tadalafil online mastercard was Grandmaster Bent Larsen, one viagra of the strongest players of his generation. This video will show you how to handle the herb viagra unusual positions and play an interesting game with good chances of a win.
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General Guide to the Opening: f4 against the Sicilian by IM Andrew Martin
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BMW has released a short video that shows off its i-brand electric and hybrid cars on the streets of Chicago.
Both the i3 and i8 concepts roll through the Windy City as BMW touts their practicality and appeal to city dwellers. The video also shows a mobile-phone service called DriveNow that locates parking, plug-in charging locations and food and entertainment points.
The BMW i3 city car will be available in 2013, and the sportier i8 is to arrive in 2014.
Check out Autoweek's inside look at the BMW i3 concept and the BMW i8 concept by Germany correspondent Greg Kable.


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Where science meets sweetness!
Our stunning range of individual desserts.
Chef Razza working hard as always!
More delicious treats.
Mazza our chocolate spray girl - we have now built a special room in the studio for all her spraying needs.
We have a huge selection of large cakes also on offer - or you could design your own with us!!
What a week! Finally after a few false starts and a couple of years in the planning we completed our first week of trading. We had a sensational response from old and new friends and we want to take this opportunity to express our gratitude for all of the custom in week 1. We thoroughly enjoyed creating some pretty spectacular dessert designs and we are really enjoying our new kitchen space. The Studio is looking great and we plan on making regular changes in the design of the store, edible art, product range and desserts so please come back as often as possible. There a some fantastic Burch & Purchese events coming up in the near future that we will tell you about in the next post and we are planning a few surprises in the Studio as well so it is exciting times and we are happy to be your first choice for cake designs. We will update this blog on a regular basis from now on, twice or three times a week will be the standard as we have so much to say! Thanks again to all who supported and we look forward to welcoming you into Melbourne's newest Sweet Studio.
647 Chapel Street, South Yarra, 3141
03 9827 7060
Tues - Sun 10.00 - 18.30
Late night Thursday cake consultation by appointment


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Have a look here and see what is your level: Learn English - Help for English Students and Learners - UsingEnglish.com
how do I use this site to improve my english. isn't there an order to use the links? thee is so much content and i dont know where to begin. i like order in my things and want to have a plan how to learn from this site.
thank you all!
Have a look here and see what is your level: Learn English - Help for English Students and Learners - UsingEnglish.com
i think u didn't understand me. i wanted to know how should i use this site. there is a lot of stuff here that i dont know. but when i'm coming to learn, how should i built myself an effective lesson? i guess it should have:
1) grammar part.
2) reading comprehensive part (maybe an article? please suggest another ways to work on my comprehensive).
3) vocabulary (but how should i learn it if i want to remember it for a long time?)
and there's another 31 subjects in this page:
what subjects are most important and where i should start in every subject??
im asking this not just for me. i want to teach my little brother english and I dont know where to start with him (till now he know past\present simple\progressive and he has a little vocabulary).
btw - thanks for ur comment,
freindly urs,
Amir Tz.
Last edited by bordos; 07-Feb-2011 at 11:34.


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I just ordered The Art of Fermentation by Sandor Katz. I can't wait to flip through the tome, mouth watering or nose wrinkling at the various fermented creations to be found within. I admit I'm taking the whole fermenting thing slow. I've experimented with quite a few recipes in Katz' primer, Wild Fermentation, and have jars of yogurt, kimchi, kraut, kombucha, and pickles in my stash. I figure I'll perfect my skills with the basics before moving to stuff like Chicha (read the recipe- I dare you) and whatever else might be awaiting in Katz' new book. But I love my kombucha. Making it yourself is not only much cheaper but you can create the flavors and sweetness that appeal to you! Besides, who can resist the science-experiment-like draw of this mushroom/yeast bevvie? Here's how I make my kombucha (based on the recipe in Wild Fermentation) (I usually double or quadruple the recipe I drink so much!):
Grab a 1 quart mason jar. Steep 2 black tea bags in 1 quart of hot water for at least 20 minutes. Remove tea bags. Add 1/4 cup sugar and stir until dissolved. Let cool to the point where you can stick your hand in without it hurting. (Very scientific) About 100 degrees. Add a kombucha mother (get one from a friend or buy at a place like OB People's Co-op), translucent side down, along with some of the kombucha the mother was stored in (or apple cider vinegar in a pinch). Cover mouth of jar with cheesecloth and store in a warm spot (70-85 degrees). Let it hang out for about a week, longer if you want it less sweet, more acidic. Once it tastes good to you, store it covered in the fridge. Start a new batch and add one of the mothers (the mother you used will grow another "skin." Peel this off and use either one.) Enjoy!
If you want to meet Sandor Katz in person and attend a bunch of cool workshops, check out this festival happening up north on September 16th: http://www.farmtofermentation.com/
Also, go to the San Diego Fermenters Club Facebook page and like 'em to hear about local meetings and events: http://www.facebook.com/fermenters


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Compliance – Reporting Path System
The Reporting Path System of SEEBURGER gives you the opportunity to inform us about violations of legal regulations and / or compliance rules and thus to contribute to their disclosure.
Compliance with legal requirements and internal compliance rules is a top priority for SEEBURGER. Violations must be recognized at an early stage in order to initiate appropriate countermeasures and to prevent possible damage for customers, employees, business partners and the company.
Severe violations in the company
SEEBURGER has set up several reporting paths in order to be able to find out about serious breaches in the company in a timely manner and to provide appropriate information. Both employees of SEEBURGER and external persons can provide information on potential bribery, fraud, antitrust violations, violations of the law on money laundering or the violation of accounting rules.
Possible reporting paths
If you have concrete or well-founded indications of serious legal violations or violations of regulations at SEEBURGER or you suspect, you have the following possibilities:
1. Corporate Compliance Officer, Christoph Stäb
- by telephone: +49(0)7252 / 96 - 1279
- by mobile telephone: +49(0)174 / 3479 660
- by e-mail: firstname.lastname@example.com
Also anonymous hints are possible. In such a case, please provide as much details as possible and, if available, documents that support your suspicion. Only if there are sufficiently concrete investigations and reasonable grounds for suspecting, your indication can ultimately effect something.
2. Compliance Lawyer of the chamber Ebner Stolz, Mr. Andreas Rupp
- by post: Ebner Stolz, RA / StB Andreas Rupp, Lorenzstr. 29, 76135 Karlsruhe, Germany
- by telephone: +49(0)721 / 915705 - 20
- by mobile telephone: +49(0)162 / 4054820
- by fax: +49(0)721 / 915705 - 99
- by e-mail: firstname.lastname@example.com
SEEBURGER follows all the indications. In the context of their processing, the highest confidentiality and fairness in dealing with the advisor is ensured. This also applies to employees who are affected by an allegation.
Last Update: 08.06.2017


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Activist hedge fund ValueAct Capital took a $2 billion stake in Microsoft, its CEO Jeffery Ubben announced at an investment a conference in New York, today.
He explained the investment by saying, "In three to five years, which is our time horizon, we'll stop talking about PC cycles and instead talk about Microsoft as the largest cloud-computing company in the world."
For his sake, let's hope so. The PC business is imploding, so Microsoft's traditionally lucrative Windows business is flattening, and could start shrinking soon.
Microsoft has two other businesses that are doing well — Servers and Tools and the Business Division, which is home to Office. Those businesses are strong enough to offset Windows, for now.
Microsoft's stock has been flat for the longest time. A lot of investors have been tempted by it, believing there is value to be unlocked. So far, they've been wrong.
Microsoft is up 12% year to date, and rose 4% on today's news. It closed at $30.83.
ValueAct describes itself as a fund "that combines intensive due diligence, a concentrated number of investments, and active, constructive involvement in the value creation at those investments."
It has $10 billion in assets under management and it "concentrates on acquiring significant ownership stakes in a limited number of companies that it believes are fundamentally undervalued."
Ubben says ValueAct will not do any campaigning to change Microsoft's strategy, according to Reuters.
A Microsoft spokesperson gave us this comment on ValueAct: "Microsoft's Board of Directors and management team welcome the perspectives of shareholders. We are committed to enhancing value for all shareholders, and will continue to take actions that we believe will enable us to achieve this objective."
Get the latest Microsoft stock price here.


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Hard to keep to 100 km/h it may be, but the 2013 Mini Roadster wasn't the only fast car on the Pork Pie Charity Run from Kaitaia to Invercargill.
The field of 47 cars encompassed classics from five decades of production of the old Mini, plus a good selection of more modern Minis, including Driven's Roadster, kindly provided by BMW Group NZ.
The Minis included a 1965 Morris 850 belonging to Waikato couple Zane and Vickie Begovich, who were content to putter along at an ideal cruising speed of about 85km/h. And there was still a nod to the famous peppy road car Minis of old which also dominated the racetracks of Europe.
Both old and new Minis seemed to attract an affectionate response along the way, there being many fans of both kinds of car among the public.
The last three times the charity run has been held the run has dropped in to the National Park service station featured in Goodbye Pork Pie, the movie which gave its name to the rally.
Coincidentally, even before he had heard of the charity run, the owner of the station, Dhruv Dewan and his wife, Nalini, had used the movie as a travel route to see New Zealand during their honeymoon following their wedding in 2008.
The 2013 run provided another honeymoon experience, this time for the recently married Bryce and Debs Mason. However, Bryce and Debs' journey was not without its challenges, as their car broke down in Whangarei on Good Friday and needed a rotor to continue.
"It would have been a quick trip to Repco and back on the road any other day, but on a public holiday it was a real mission to fix it," Debs said.
"Luckily the 'Mini grapevine' was activated, after a few texts and phone calls we were put in touch with a Mini owner in Whangarei who was happy to loan us his rotor."
There were many more cases of borrowing and swapping along the route of the run; for instance at the Classics Museum in Frankton, which has many Minis on display including a replica of the one featured in the movie.
Alan and Sandy Williams needed running repairs and the museum kindly supplied an engine bolt out of their Pork Pie replica car to get the couple back on the road.
The charity run attracted much attention, which helped when the buckets came out to raise money for this year's charity, Leukaemia & Blood Cancer New Zealand.
The donation which sticks in the mind for me was on State Highway 1, between Kaitaia and Whangarei, where we took several gold coins off a friendly police officer who had stopped us for a donation to something called "The Consolidated Fund" - fair cop.
One way or another the generosity of Kiwis was staggering, with $165,000 raised for this worthy cause.
To donate go to porkpie.co.nz/view_group_event_profile/470


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Camino Ruiz Square
Office Info
- Mon – Tue: 9:00 AM - 6:00 PM
- Wed: 10:00 AM - 6:00 PM
- Thu – Sat: 9:00 AM - 6:00 PM
- Sun: Closed
Apartment Features
- Air Conditioner
- Patio/ Balcony
- Cable Ready
- Ceiling fan
- Dish Washer
- Disposal
- Dryer
- Large closets
- Microwave
- Patio
- Refrigerator
- View
- Washer
- Window Coverings
Community Amenities
- Fitness center
- High Speed Internet Available
- Laundry
- Near Mass Transit
- On-site Maintenance
- On-site management
- Package Receiving
- Parking
- Pet friendly
- Pool
- Spa
- Storage Space
Pet Policy
- We allow cats and dogs
We love all pets, but the following breeds/crossbreeds are not allowed: Pit Bulls (Staffordshire Bull Terrier), Dobermans, Rottweilers, Chow Chows, German Shepherds, Huskies, Mastiffs, Great Danes, Malamutes, Akitas and Wolf Hybrids. Breed restrictions are subject to change without notice.
- Monthly Pet Rent: Dogs $60/Cats $40
- Deposit: $500 (for up to 2 pets)
Floor Plans and Pricing
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*Branding elements, floor plans, layout plans, specifications, images, names, drawings, perspectives, models, graphics, logos, icons and other details herein are only indicative and the Developer/Promoter/Owner reserves the right to change all or any of them. All room dimensions are approximate only and may or may not include balcony square feet in total square footage. Prices and availability are subject to change. Prices vary based on move-in and lease terms.
*The monthly rental rates provided on our website are an estimate of the likely rental rate for the available floorplans and provided as a service to prospective residents. We cannot guarantee that a rental rate displayed above will be the actual rate offered at the time a rental agreement is signed as our rates change daily based on economic factors of the community such as unit availability.
Leasing Details
- Deposit:$500
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- Application Fee:$48
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With our beloved Madiba critically ill in hospital, visiting Robben Island yesterday was an even more moving experience than expected. I wish I knew more of the history behind some of the photographic images I encountered along our walk. Who were these tortured faces? What had they been convicted of? However, it was profoundly significant to see the tiny cell where Mandela spent 18 years of his life. He may have been shut away, but his spirit and conviction could never be snuffed out...
|Prisoners arriving by boat
|The release of political prisoners in 1991
A rather bizarre image below. Christmas on Robben Island?
|Double ammunition
|Prisoners on Robben Island
|Views from Robben Island of Cape Town
|Kramat on Robben Island
The 'crime' many Political Leaders were 'put away' for - Sabotage...
|Prisoner ID card (Billy Nair)
|My daughter and friend in the courtyard outside Nelson Mandela's cell (Section B)
|Sign post
|Cell 5 where prisoner 466/64 remained for 18 years
|A mat (no mattress) for Nelson Mandela to sleep on
|Watch Tower
|Returning 'home' on the ferry
|A return visit years later (Telegraph)
I am fundamentally an optimist. Whether that comes from nature or nurture, I cannot say. Part of being optimistic is keeping one's head pointed toward the sun, one's feet moving forward. There were many dark moments when my faith in humanity was sorely tested, but I would not and could not give myself up to despair. That way lays defeat and death.
― Nelson Mandela, Long Walk to Freedom: Autobiography of Nelson Mandela
(Unless otherwise stated, all photographs by Philippa Berrington-Blew)


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Wednesday, January 28, 2009
It gives me great joy...
Cheers to all of my fellow Wine Century Club members!
7 comments:
- Edward said...
Well done Joseph St Thomas!
- January 29, 2009 9:10 AM
- Marcus said...
But you are still hiding your name? Is this because of that phase where you almost moved to Toronto?
- January 29, 2009 7:10 PM
- Shea said...
Nice :).
- February 02, 2009 2:42 AM
- Joe said...
Hi Ed, everyone knows I am a Saint.
Yes Marcus, I have to keep up the mystery.
Thanks Shea - when do you go for it?
Cheers all, I think I will go for Teroldego tonight...
- February 04, 2009 5:31 PM
- Barry said...
Joe...are you getting paid by the Burgundians?
I'd insist on a DRC!
- February 06, 2009 11:44 AM
- David said...
Congrats! reminds me I need to update my Century Club tracker. And I'm planning on opening a schiava based red tonight to get a bit closer.
- February 07, 2009 11:15 AM
- Joe said...
Barry - I was going to let this shameless self-promotion slide, but then he started polluting other posts - all he had to do was ask for a link, now I just delete him.
Hi David - never had a schiava-based wine, I may have to target the "two century" club.
- February 07, 2009 11:26 AM


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Bogaerts not wilting under stage's harshest lights
BOSTON -- Xander Bogaerts never could have envisioned how his season was going to play out when he reported to Spring Training in February.
The 21-year-old Aruban phenom was the prized asset of Boston's deep Minor League system, but he appeared to be at least another full year away from making any type of impact at the big league level.View Full Game Coverage
BOSTON -- Xander Bogaerts never could have envisioned how his season was going to play out when he reported to Spring Training in February.
The 21-year-old Aruban phenom was the prized asset of Boston's deep Minor League system, but he appeared to be at least another full year away from making any type of impact at the big league level.View Full Game Coverage
A lot has changed since then, though. Bogaerts continued his ascension through the ranks at a rapid pace and now finds himself as the youngest player to start a postseason game in Red Sox history.
"Wow, it's a crazy year, I would say," Bogaerts said when asked to reflect on his improbable run through professional baseball. "Very blessed. I mean, sometimes I can't even believe I'm here -- at 21 and starting in Double-A, and now here in the [American League Championship Series], one game away from the World Series. Sometimes it's hard to believe, but it's good so far."
Bogaerts entered the season as the 20th-best prospect in baseball as ranked by MLB.com. There was very little doubt he would eventually play a role in Boston's plans, but the timing remained uncertain.
Boston already had Stephen Drew and Jose Iglesias splitting time at shortstop, and Will Middlebrooks began the season as a seemingly permanent fixture at third. That didn't bode well for Bogaerts' chances in the big leagues, but that was just fine, considering he started the year with just 23 games above Class A ball under his belt.
There was a need for more development in the Minors, but Bogaerts certainly didn't make things easy for the Boston brass. He forced a promotion to Triple-A Pawtucket after hitting .311 with an impressive .909 OPS in 56 games, then proceeded to continue that type of success at that level.
An opportunity then presented itself when Iglesias was dealt to the Tigers as part of a three-way deal prior to the non-waiver Trade Deadline. That opened a spot on the bench, and within a few weeks, Bogaerts received the news that he was heading to Boston.
He understandably didn't get off to a fast start, as he struggled to receive everyday at-bats while at the same time adjusting to Major League pitching. He proceeded to hit just .250, but he added three extra-base hits and impressed his teammates by how at ease he seemed to be in the spotlight.
"He's always under control," second baseman Dustin Pedroia said. "It feels like he's been in the big leagues for 10 years. Thinking out situations. Great approach at the plate. He's going to be good for a long time."
Bogaerts now finds himself under an even more powerful microscope, as he has suddenly emerged as a viable starting position player in the ALCS vs. Detroit. His chance came in Game 5, when he received the start at third base over the struggling Middlebrooks, who is just 4-for-23 during the postseason.
It would have been understandable if nerves took over, but Bogaerts looked right at home. He hit a key double in the second inning off Tigers starter Anibal Sanchez and later turned a crucial inning-ending double play on a ball hit by speedy outfielder Austin Jackson.
Bogaerts had doubled in Game 4 of the ALCS when he came off the bench as a defensive replacement for pinch-hitter Mike Carp. That makes him one of just six players to record multiple extra-base hits in an LCS before his 22nd birthday, a group that also features Wayne Garrett (1969, Mets), Chris Speier (1971, Giants), Gregg Jefferies (1988, Mets), Miguel Cabrera (2003, Marlins) and Justin Upton (2007, D-backs).
Bogaerts' recent performance has earned him another start at third base, in the potential deciding Game 6 at Fenway Park on Saturday at 8 p.m. ET on FOX.
Manager John Farrell confirmed the decision during a news conference on Friday afternoon and had nothing but positive things to say about his surprise contributor.
"It's definitely special," Bogaerts said. "I want the manager to have confidence in me, especially in the playoffs. Every game is important, every at-bat. It's definitely huge."
Bogaerts will have it tough with Max Scherzer on the mound for Detroit, but the challenge won't be any more difficult than all the others he's already overcome this season.
So his unlikely ride continues, and he intends to enjoy it every step of the way. He knows what's at stake, but his confidence only appears to be rising, and the timing couldn't be any better for a Boston organization that is just one win away from reaching baseball's biggest stage.
"I try to have fun," he said. "That's the one thing I always do when I play good -- have fun. Baseball is the one thing I know how to do good, so have fun while you're doing it.
"We're going up against a tough pitcher. We also have [Clay] Buchholz. Buchholz versus Scherzer is a good matchup. Whoever makes less mistakes wins. That's all I can say."
Gregor Chisholm is a reporter for MLB.com. Read his blog, North of the Border, and follow him on Twitter @gregorMLB.


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Summary: Adenosine-deaminase (editase) domain
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Adenosine deaminase Edit Wikipedia article
|Adenosine/AMP deaminase
crystal structure of plasmodium yoelii adenosine deaminase (py02076)
|Pfam clan
|Adenosine deaminase (editase) domain
|Adenosine/AMP deaminase N-terminal
Adenosine deaminase (also known as adenosine aminohydrolase, or ADA) is an enzyme (EC 184.108.40.206) involved in purine metabolism. It is needed for the breakdown of adenosine from food and for the turnover of nucleic acids in tissues.
Its primary function in humans is the development and maintenance of the immune system.[5] However, the full physiological role of ADA is not yet completely understood.[6]
ADA exists in both small form (as a monomer) and large form (as a dimer-complex).[6] In the monomer form, the enzyme is a polypeptide chain,[7] folded into eight strands of parallel α/β barrels, which surround a central deep pocket that is the active site.[5] In addition to the eight central β-barrels and eight peripheral α-helices, ADA also contains five additional helices: residues 19-76 fold into three helices, located between β1 and α1 folds; and two antiparallel carboxy-terminal helices are located across the amino-terminal of the β-barrel.
The ADA active site contains a zinc ion, which is located in the deepest recess of the active site and coordinated by five atoms from His15, His17, His214, Asp295, and the substrate.[5] Zinc is the only cofactor necessary for activity.
The substrate, adenosine, is stabilized and bound to the active site by nine hydrogen bonds.[5] The carboxyl group of Glu217, roughly coplanar with the substrate purine ring, is in position to form a hydrogen bond with N1 of the substrate. The carboxyl group of Asp296, also coplanar with the substrate purine ring, forms hydrogen bond with N7 of the substrate. The NH group of Gly184 is in position to form a hydrogen bond with N3 of the substrate. Asp296 forms bonds both with the Zn2+ ion as well as with 6-OH of the substrate. His238 also hydrogen bonds to substrate 6-OH. The 3'-OH of the substrate ribose forms a hydrogen bond with Asp19, while the 5'-OH forms a hydrogen bond with His17. Two further hydrogen bonds are formed to water molecules, at the opening of the active site, by the 2'-OH and 3'-OH of the substrate.
Due to the recessing of the active site inside the enzyme, the substrate, once bound, is almost completely sequestered from solvent.[5] The surface exposure of the substrate to solvent when bound is 0.5% the surface exposure of the substrate in the free state.
ADA irreversibly deaminates adenosine, converting it to the related nucleoside inosine by the substitution of the amino group for a keto group.
Inosine can then be deribosylated (removed from ribose) by another enzyme called purine nucleoside phosphorylase (PNP), converting it to hypoxanthine.
Mechanism of catalysis
The proposed mechanism for ADA-catalyzed deamination is stereospecific addition-elimination via tetrahedral intermediate.[8] By either mechanism, Zn2+ as a strong electrophile activates a water molecule, which is deprotonated by the basic Asp295 to form the attacking hydroxide.[5] His238 orients the water molecule and stabilizes the charge of the attacking hydroxide. Glu217 is protonated to donate a proton to N1 of the substrate.
The reaction is stereospecific due to the location of the zinc, Asp295, and His238 residues, which all face the B-side of the purine ring of the substrate.[5]
Competitive inhibition has been observed for ADA, where the product inosine acts at the competitive inhibitor to enzymatic activity.[9]
ADA is considered one of the key enzymes of purine metabolism.[8] The enzyme has been found in bacteria, plants, invertebrates, vertebrates, and mammals, with high conservation of amino acid sequence.[6] The high degree of amino acid sequence conservation suggests the crucial nature of ADA in the purine salvage pathway.
Primarily, ADA in humans is involved in the development and maintenance of the immune system. However, ADA association has also been observed with epithelial cell differentiation, neurotransmission, and gestation maintenance.[10] It has also been proposed that ADA, in addition to adenosine breakdown, stimulates release of excitatory amino acids and is necessary to the coupling of A1 adenosine receptors and heterotrimeric G proteins.[6] Adenosine deaminase deficiency leads to pulmonary fibrosis,[11] suggesting that chronic exposure to high levels of adenosine can exacerbate inflammation responses rather than suppressing them. It has also been recognized that adenosine deaminase protein and activity is upregulated in mouse hearts that overexpress HIF-1 alpha, which in part explains the attenuated levels of adenosine in HIF-1 alpha expressing hearts during ischemic stress.[12]
Some mutations in the gene for adenosine deaminase cause it not to be expressed. The resulting deficiency is one cause of severe combined immunodeficiency (SCID), particularly of autosomal recessive inheritance.[13] Deficient levels of ADA have also been associated with pulmonary inflammation, thymic cell death, and defective T-cell receptor signaling.[14][15]
Conversely, mutations causing this enzyme to be overexpressed are one cause of hemolytic anemia .[16]
There is some evidence that a different allele (ADA2) may lead to autism.[17]
Elevated levels of ADA has also been associated with AIDS.[14][18]
There are 2 isoforms of ADA: ADA1 and ADA2.
- ADA1 is found in most body cells, particularly lymphocytes and macrophages, where it is present not only in the cytosol and nucleus but also as the ecto- form on the cell membrane attached to dipeptidyl peptidase-4 (aka, CD26). ADA1 is involved mostly in intracellular activity, and exists both in small form (monomer) and large form (dimer).[6] The interconversion of small to large forms is regulated by a 'conversion factor' in the lung.[19]
- ADA2 was first identified in human spleen.[20] It was subsequently found in other tissues including the macrophage where it co-exists with ADA1. The two isoforms regulate the ratio of adenosine to deoxyadenosine potentiating the killing of parasites. ADA2 is found predominantly in the human plasma and serum, and exists solely as a homodimer.[21]
Clinical significance
ADA2 is the predominant form present in human blood plasma and is increased in many diseases, particularly those associated with the immune system: for example rheumatoid arthritis, psoriasis, and sarcoidosis. The plasma ADA2 isoform is also increased in most cancers. ADA2 is not ubiquitous but co-exists with ADA1 only in monocytes-macrophages.[citation needed]
Total plasma ADA can be measured using high performance liquid chromatography or enzymatic or colorimetric techniques. Perhaps the simplest system is the measurement of the ammonia released from adenosine when broken down to inosine. After incubation of plasma with a buffered solution of adenosine the ammonia is reacted with a Berthelot reagent to form a blue colour which is proportionate to the amount of enzyme activity. To measure ADA2, erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA) is added prior to incubation so as to inhibit the enzymatic activity of ADA1.[20] It is the absence of ADA1 that causes SCID.
ADA can also be used in the workup of lymphocytic pleural effusions or peritoneal ascites, in that such specimens with low ADA levels essentially excludes tuberculosis from consideration.[22]
Tuberculosis pleural effusions can now be diagnosed accurately by increased levels of pleural fluid adenosine deaminase, above 40 U per liter.[23]
Cladribine is an anti-neoplastic agent used in the treatment of hairy cell leukemia; its mechanism of action is inhibition of adenosine deaminase.
Coformycin was also described as a adenosine deaminase inhibitor but is alleged to be an antibiotic.
See also
- ^ a b c GRCh38: Ensembl release 89: ENSG00000196839 - Ensembl, May 2017
- ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000017697 - Ensembl, May 2017
- ^ "Human PubMed Reference:".
- ^ "Mouse PubMed Reference:".
- ^ a b c d e f g Wilson DK, Rudolph FB, Quiocho FA (May 1991). "Atomic structure of adenosine deaminase complexed with a transition-state analog: understanding catalysis and immunodeficiency mutations". Science. 252 (5010): 1278–1284. doi:10.1126/science.1925539. PMID 1925539.
- ^ a b c d e Cristalli G, Costanzi S, Lambertucci C, Lupidi G, Vittori S, Volpini R, Camaioni E (Mar 2001). "Adenosine deaminase: functional implications and different classes of inhibitors". Medicinal Research Reviews. 21 (2): 105–128. doi:10.1002/1098-1128(200103)21:2<105::AID-MED1002>3.0.CO;2-U. PMID 11223861.
- ^ Daddona PE, Kelley WN (Jan 1977). "Human adenosine deaminase. Purification and subunit structure". The Journal of Biological Chemistry. 252 (1): 110–115. PMID 13062.
- ^ a b Losey HC, Ruthenburg AJ, Verdine GL (Jan 2006). "Crystal structure of Staphylococcus aureus tRNA adenosine deaminase TadA in complex with RNA". Nature Structural & Molecular Biology volume. 13 (2): 153–159. doi:10.1038/nsmb1047.
- ^ Saboury AA, Divsalar A, Jafari GA, Moosavi-Movahedi AA, Housaindokht MR, Hakimelahi GH (May 2002). "A product inhibition study on adenosine deaminase by spectroscopy and calorimetry". Journal of Biochemistry and Molecular Biology. 35 (3): 302–305. doi:10.5483/BMBRep.2002.35.3.302. PMID 12297022.
- ^ Moriwaki Y, Yamamoto T, Higashino K (Oct 1999). "Enzymes involved in purine metabolism--a review of histochemical localization and functional implications". Histology and Histopathology. 14 (4): 1321–1340. PMID 10506947.
- ^ Blackburn MR (2003). "Too much of a good thing: adenosine overload in adenosine-deaminase-deficient mice". Trends in Pharmacological Sciences. 24 (2): 66–70. doi:10.1016/S0165-6147(02)00045-7. PMID 12559769.
- ^ Wu J, Bond C, Chen P, Chen M, Li Y, Shohet RV, Wright G (2015). "HIF-1α in the heart: remodeling nucleotide metabolism". Journal of Molecular and Cellular Cardiology. 82: 194–200. doi:10.1016/j.yjmcc.2015.01.014. PMC 4405794 . PMID 25681585.
- ^ Sanchez JJ, Monaghan G, Børsting C, Norbury G, Morling N, Gaspar HB (May 2007). "Carrier frequency of a nonsense mutation in the adenosine deaminase (ADA) gene implies a high incidence of ADA-deficient severe combined immunodeficiency (SCID) in Somalia and a single, common haplotype indicates common ancestry". Annals of Human Genetics. 71 (Pt 3): 336–47. doi:10.1111/j.1469-1809.2006.00338.x. PMID 17181544.
- ^ a b Blackburn MR, Kellems RE (2005). "Adenosine deaminase deficiency: metabolic basis of immune deficiency and pulmonary inflammation". Advances in Immunology. Advances in Immunology. 86: 1–41. doi:10.1016/S0065-2776(04)86001-2. ISBN 9780120044863. PMID 15705418.
- ^ Apasov SG, Blackburn MR, Kellems RE, Smith PT, Sitkovsky MV (Jul 2001). "Adenosine deaminase deficiency increases thymic apoptosis and causes defective T cell receptor signaling". The Journal of Clinical Investigation. 108 (1): 131–141. doi:10.1172/JCI10360. PMC 209335 . PMID 11435465.
- ^ Chottiner EG, Cloft HJ, Tartaglia AP, Mitchell BS (Mar 1987). "Elevated adenosine deaminase activity and hereditary hemolytic anemia. Evidence for abnormal translational control of protein synthesis". The Journal of Clinical Investigation. 79 (3): 1001–5. doi:10.1172/JCI112866. PMC 424261 . PMID 3029177.
- ^ Persico AM, Militerni R, Bravaccio C, Schneider C, Melmed R, Trillo S, Montecchi F, Palermo MT, Pascucci T, Puglisi-Allegra S, Reichelt KL, Conciatori M, Baldi A, Keller F (Dec 2000). "Adenosine deaminase alleles and autistic disorder: case-control and family-based association studies". American Journal of Medical Genetics. 96 (6): 784–90. doi:10.1002/1096-8628(20001204)96:6<784::AID-AJMG18>3.0.CO;2-7. PMID 11121182.
- ^ Cowan MJ, Brady RO, Widder KJ (Feb 1986). "Elevated erythrocyte adenosine deaminase activity in patients with acquired immunodeficiency syndrome". Proceedings of the National Academy of Sciences of the United States of America. 83 (4): 1089–1091. doi:10.1073/pnas.83.4.1089. PMC 323016 . PMID 3006027.
- ^ Schrader WP, Stacy AR (Sep 1977). "Purification and subunit structure of adenosine deaminase from human kidney". The Journal of Biological Chemistry. 252 (18): 6409–6415. PMID 893413.
- ^ a b Schrader WP, Pollara B, Meuwissen HJ (Jan 1978). "Characterization of the residual adenosine deaminating activity in the spleen of a patient with combined immunodeficiency disease and adenosine deaminase deficiency". Proceedings of the National Academy of Sciences of the United States of America. 75 (1): 446–50. doi:10.1073/pnas.75.1.446. PMC 411266 . PMID 24216.
- ^ Zavialov AV, Engström A (Oct 2005). "Human ADA2 belongs to a new family of growth factors with adenosine deaminase activity". The Biochemical Journal. 391 (Pt 1): 51–57. doi:10.1042/BJ20050683. PMC 1237138 . PMID 15926889.
- ^ Jiménez Castro D, Díaz Nuevo G, Pérez-Rodríguez E, Light RW (2003). "Diagnostic value of adenosine deaminase in nontuberculous lymphocytic pleural effusions" (PDF). Eur. Respir. J. 21 (2): 220–4. doi:10.1183/09031936.03.00051603. PMID 12608433.
- ^ Brunicardi F, Andersen D, Billiar T, Dunn D, Hunter J, Pollock RE (2005). "Chapter 18, question 16". Schwartz's principles of surgery (8th ed.). New York: McGraw-Hill Professional. ISBN 978-0071410908.
Further reading
- da Cunha JG (1992). "[Adenosine deaminase. A pluridisciplinary enzyme]". Acta Médica Portuguesa. 4 (6): 315–23. PMID 1807098.
- Franco R, Casadó V, Ciruela F, Saura C, Mallol J, Canela EI, Lluis C (Jul 1997). "Cell surface adenosine deaminase: much more than an ectoenzyme". Progress in Neurobiology. 52 (4): 283–94. doi:10.1016/S0301-0082(97)00013-0. PMID 9247966.
- Valenzuela A, Blanco J, Callebaut C, Jacotot E, Lluis C, Hovanessian AG, Franco R (1997). "HIV-1 envelope gp120 and viral particles block adenosine deaminase binding to human CD26". Advances in Experimental Medicine and Biology. 421: 185–92. doi:10.1007/978-1-4757-9613-1_24. PMID 9330696.
- Moriwaki Y, Yamamoto T, Higashino K (Oct 1999). "Enzymes involved in purine metabolism--a review of histochemical localization and functional implications". Histology and Histopathology. 14 (4): 1321–40. PMID 10506947.
- Hirschhorn R (1993). "Identification of two new missense mutations (R156C and S291L) in two ADA- SCID patients unusual for response to therapy with partial exchange transfusions". Human Mutation. 1 (2): 166–8. doi:10.1002/humu.1380010214. PMID 1284479.
- Berkvens TM, van Ormondt H, Gerritsen EJ, Khan PM, van der Eb AJ (Aug 1990). "Identical 3250-bp deletion between two AluI repeats in the ADA genes of unrelated ADA-SCID patients". Genomics. 7 (4): 486–90. doi:10.1016/0888-7543(90)90190-6. PMID 1696926.
- Aran JM, Colomer D, Matutes E, Vives-Corrons JL, Franco R (Aug 1991). "Presence of adenosine deaminase on the surface of mononuclear blood cells: immunochemical localization using light and electron microscopy". The Journal of Histochemistry and Cytochemistry. 39 (8): 1001–8. doi:10.1177/39.8.1856451. PMID 1856451.
- Bielat K, Tritsch GL (Apr 1989). "Ecto-enzyme activity of human erythrocyte adenosine deaminase". Molecular and Cellular Biochemistry. 86 (2): 135–42. doi:10.1007/BF00222613. PMID 2770711.
- Hirschhorn R, Tzall S, Ellenbogen A, Orkin SH (Feb 1989). "Identification of a point mutation resulting in a heat-labile adenosine deaminase (ADA) in two unrelated children with partial ADA deficiency". The Journal of Clinical Investigation. 83 (2): 497–501. doi:10.1172/JCI113909. PMC 303706 . PMID 2783588.
- Murray JL, Perez-Soler R, Bywaters D, Hersh EM (Jan 1986). "Decreased adenosine deaminase (ADA) and 5'nucleotidase (5NT) activity in peripheral blood T cells in Hodgkin disease". American Journal of Hematology. 21 (1): 57–66. doi:10.1002/ajh.2830210108. PMID 3010705.
- Wiginton DA, Kaplan DJ, States JC, Akeson AL, Perme CM, Bilyk IJ, Vaughn AJ, Lattier DL, Hutton JJ (Dec 1986). "Complete sequence and structure of the gene for human adenosine deaminase". Biochemistry. 25 (25): 8234–44. doi:10.1021/bi00373a017. PMID 3028473.
- Akeson AL, Wiginton DA, Dusing MR, States JC, Hutton JJ (Nov 1988). "Mutant human adenosine deaminase alleles and their expression by transfection into fibroblasts". The Journal of Biological Chemistry. 263 (31): 16291–6. PMID 3182793.
- Glader BE, Backer K (Feb 1988). "Elevated red cell adenosine deaminase activity: a marker of disordered erythropoiesis in Diamond-Blackfan anaemia and other haematologic diseases". British Journal of Haematology. 68 (2): 165–8. doi:10.1111/j.1365-2141.1988.tb06184.x. PMID 3348976.
- Petersen MB, Tranebjaerg L, Tommerup N, Nygaard P, Edwards H (Feb 1987). "New assignment of the adenosine deaminase gene locus to chromosome 20q13 X 11 by study of a patient with interstitial deletion 20q". Journal of Medical Genetics. 24 (2): 93–6. doi:10.1136/jmg.24.2.93. PMC 1049896 . PMID 3560174.
- Orkin SH, Goff SC, Kelley WN, Daddona PE (Apr 1985). "Transient expression of human adenosine deaminase cDNAs: identification of a nonfunctional clone resulting from a single amino acid substitution". Molecular and Cellular Biology. 5 (4): 762–7. PMC 366780 . PMID 3838797.
- Valerio D, Duyvesteyn MG, Dekker BM, Weeda G, Berkvens TM, van der Voorn L, van Ormondt H, van der Eb AJ (Feb 1985). "Adenosine deaminase: characterization and expression of a gene with a remarkable promoter". The EMBO Journal. 4 (2): 437–43. PMC 554205 . PMID 3839456.
- Bonthron DT, Markham AF, Ginsburg D, Orkin SH (Aug 1985). "Identification of a point mutation in the adenosine deaminase gene responsible for immunodeficiency". The Journal of Clinical Investigation. 76 (2): 894–7. doi:10.1172/JCI112050. PMC 423929 . PMID 3839802.
- Daddona PE, Shewach DS, Kelley WN, Argos P, Markham AF, Orkin SH (Oct 1984). "Human adenosine deaminase. cDNA and complete primary amino acid sequence". The Journal of Biological Chemistry. 259 (19): 12101–6. PMID 6090454.
- Valerio D, Duyvesteyn MG, Meera Khan P, Geurts van Kessel A, de Waard A, van der Eb AJ (Nov 1983). "Isolation of cDNA clones for human adenosine deaminase". Gene. 25 (2–3): 231–40. doi:10.1016/0378-1119(83)90227-5. PMID 6198240.
External links
- ADA human gene location in the UCSC Genome Browser.
- ADA human gene details in the UCSC Genome Browser.
This page is based on a Wikipedia article. The text is available under the Creative Commons Attribution/Share-Alike License.
This tab holds the annotation information that is stored in the Pfam database. As we move to using Wikipedia as our main source of annotation, the contents of this tab will be gradually replaced by the Wikipedia tab.
Adenosine-deaminase (editase) domain Provide feedback
Adenosine deaminases acting on RNA (ADARs) can deaminate adenosine to form inosine. In long double-stranded RNA, this process is non-specific; it occurs site-specifically in RNA transcripts. The former is important in defence against viruses, whereas the latter may affect splicing or untranslated regions. They are primarily nuclear proteins, but a longer isoform of ADAR1 is found predominantly in the cytoplasm. ADARs are derived from the Tad1-like tRNA deaminases that are present across eukaryotes. These in turn belong to the nucleotide/nucleic acid deaminase superfamily and are characterized by a distinct insert between the two conserved cysteines that are involved in binding zinc [2].
Literature references
Keegan LP, Leroy A, Sproul D, O'Connell MA; , Genome Biol 2004;5:209.: Adenosine deaminases acting on RNA (ADARs): RNA-editing enzymes. PUBMED:14759252 EPMC:14759252
Iyer LM, Zhang D, Rogozin IB, Aravind L;, Nucleic Acids Res. 2011; [Epub ahead of print]: Evolution of the deaminase fold and multiple origins of eukaryotic editing and mutagenic nucleic acid deaminases from bacterial toxin systems. PUBMED:21890906 EPMC:21890906
External database links
|PROSITE profile:
This tab holds annotation information from the InterPro database.
InterPro entry IPR002466
Editase (EC) are enzymes that alter mRNA by catalyzing the site-selective deamination of adenosine residue into inosine residue. The editase domain contains the active site and binds three Zn atoms [PUBMED:9159072].
Several editases share a common global arrangement of domains, from N to C terminus: two 'double-stranded RNA-specific adenosine deaminase' (DRADA) repeat domains (INTERPRO), followed by three 'double-stranded RNA binding' (DsRBD) domains, followed by the editase domain. Other editases have a simplified domains structure with no DRADA_REP and possibly fewer DSRBD domains. Editase that deaminate cytidine are not detected by this signature.
Gene Ontology
The mapping between Pfam and Gene Ontology is provided by InterPro. If you use this data please cite InterPro.
|Molecular function
|RNA binding (GO:0003723)
|adenosine deaminase activity (GO:0004000)
|Biological process
|RNA processing (GO:0006396)
Domain organisation
Below is a listing of the unique domain organisations or architectures in which this domain is found. More...
The graphic that is shown by default represents the longest sequence with a given architecture. Each row contains the following information:
- the number of sequences which exhibit this architecture
a textual description of the architecture, e.g. Gla, EGF x 2, Trypsin.
This example describes an architecture with one
Gladomain, followed by two consecutive
EGFdomains, and finally a single
- a link to the page in the Pfam site showing information about the sequence that the graphic describes
- the UniProt description of the protein sequence
- the number of residues in the sequence
- the Pfam graphic itself.
Note that you can see the family page for a particular domain by clicking on the graphic. You can also choose to see all sequences which have a given architecture by clicking on the Show link in each row.
Finally, because some families can be found in a very large number of architectures, we load only the first fifty architectures by default. If you want to see more architectures, click the button at the bottom of the page to load the next set.
Loading domain graphics...
Pfam Clan
This family is a member of clan CDA (CL0109), which has the following description:
This clan contains both free nucleotide and nucleic acid deaminases that act on adenosine, cytosine, guanine and cytidine, and are collectively known as the deaminase superfamily. The conserved fold consists of a three-layered alpha/beta/alpha structure with 3 helices and 4 strands in the 2134 order [1,2].This superfamily is further divided into two major divisions based on the presence of a helix (helix-4) that renders the terminal strands (strands 4 and 5) either parallel to each other in its presence, or anti-parallel in its absence [2]. Structurally, the deaminase-like fold is present in four other superfamilies including the JAB-like metalloproteins, the C-terminal AICAR transformylase-catalyzing domains of PurH, Tm1506 and the formate dehydrogenase accessory subunit FdhD. The active site of the deaminases is composed of three residues that coordinate a zinc ion between conserved helices 2 and 3. The residues are typically found as [HCD]xE and CxxC motifs at the beginning of helices 2 and 3. The zinc ion activates a water molecule, which forms a tetrahderal intermediate with the carbon atom that is linked to the amine group. This is followed by deamination of the base.
The clan contains the following 33 members:A_deamin AICARFT_IMPCHas AID APOBEC1 APOBEC2 APOBEC3 APOBEC4 APOBEC4_like APOBEC_C APOBEC_N Bd3614-deam DAAD dCMP_cyt_deam_1 dCMP_cyt_deam_2 DYW_deaminase FdhD-NarQ Inv-AAD LmjF365940-deam LpxI_C MafB19-deam NAD1 NAD2 OTT_1508_deam Pput2613-deam SCP1201-deam SNAD1 SNAD2 SNAD3 SNAD4 TM1506 Toxin-deaminase XOO_2897-deam YwqJ-deaminase
We store a range of different sequence alignments for families. As well as the seed alignment from which the family is built, we provide the full alignment, generated by searching the sequence database (reference proteomes) using the family HMM. We also generate alignments using four representative proteomes (RP) sets, the UniProtKB sequence database, the NCBI sequence database, and our metagenomics sequence database. More...
There are various ways to view or download the sequence alignments that we store. We provide several sequence viewers and a plain-text Stockholm-format file for download.
Alignment types
We make a range of alignments for each Pfam-A family:
- seed
- the curated alignment from which the HMM for the family is built
- full
- the alignment generated by searching the sequence database using the HMM
- Representative Proteomes (RPs) at 15%, 35%, 55% and 75% co-membership thresholds
- UniProt
- alignment generated by searching the UniProtKB sequence database using the family HMM
- alignment generated by searching the NCBI sequence database using the family HMM
- meta
- alignment generated by searching the metagenomics sequence database using the family HMM
You can see the alignments as HTML or in three different sequence viewers:
- jalview
- a Java applet developed at the University of Dundee. You will need Java installed before running jalview
- an HTML page showing the whole alignment.Please note: full Pfam alignments can be very large. These HTML views are extremely large and often cause problems for browsers. Please use either jalview or the Pfam viewer if you have trouble viewing the HTML version
- PP/Heatmap
- an HTML-based representation of the alignment, coloured according to the posterior-probability (PP) values from the HMM. As for the standard HTML view, heatmap alignments can also be very large and slow to render.
You can download (or view in your browser) a text representation of a Pfam alignment in various formats:
- Selex
- Stockholm
You can also change the order in which sequences are listed in the alignment, change how insertions are represented, alter the characters that are used to represent gaps in sequences and, finally, choose whether to download the alignment or to view it in your browser directly.
You may find that large alignments cause problems for the viewers and the reformatting tool, so we also provide all alignments in Stockholm format. You can download either the plain text alignment, or a gzipped version of it.
View options
We make a range of alignments for each Pfam-A family. You can see a description of each above. You can view these alignments in various ways but please note that some types of alignment are never generated while others may not be available for all families, most commonly because the alignments are too large to handle.
|Representative proteomes
1Cannot generate PP/Heatmap alignments for seeds; no PP data available
Key: available, not generated, — not available.
Format an alignment
Download options
We make all of our alignments available in Stockholm format. You can download them here as raw, plain text files or as gzip-compressed files.
|Representative proteomes
|Raw Stockholm
You can also download a FASTA format file containing the full-length sequences for all sequences in the full alignment.
HMM logo
HMM logos is one way of visualising profile HMMs. Logos provide a quick overview of the properties of an HMM in a graphical form. You can see a more detailed description of HMM logos and find out how you can interpret them here. More...
If you find these logos useful in your own work, please consider citing the following article:
This page displays the phylogenetic tree for this family's seed alignment. We use FastTree to calculate neighbour join trees with a local bootstrap based on 100 resamples (shown next to the tree nodes). FastTree calculates approximately-maximum-likelihood phylogenetic trees from our seed alignment.
Note: You can also download the data file for the tree.
Curation and family details
This section shows the detailed information about the Pfam family. You can see the definitions of many of the terms in this section in the glossary and a fuller explanation of the scoring system that we use in the scores section of the help pages.
|Seed source:
|Previous IDs:
|Sequence Ontology:
|Mian N , Bateman A , Iyer LM , Zhang D , Aravind L
|Number in seed:
|Number in full:
|Average length of the domain:
|277.50 aa
|Average identity of full alignment:
|26 %
|Average coverage of the sequence by the domain:
|54.60 %
HMM information
|HMM build commands:
build method: hmmbuild -o /dev/null HMM SEED
search method: hmmsearch -Z 45638612 -E 1000 --cpu 4 HMM pfamseq
|Model details:
|Model length:
|Family (HMM) version:
|download the raw HMM for this family
Species distribution
Sunburst controlsHide
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|Other sequences
|Unclassified sequence
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This visualisation provides a simple graphical representation of the distribution of this family across species. You can find the original interactive tree in the adjacent tab. More...
This chart is a modified "sunburst" visualisation of the species tree for this family. It shows each node in the tree as a separate arc, arranged radially with the superkingdoms at the centre and the species arrayed around the outermost ring.
How the sunburst is generated
The tree is built by considering the taxonomic lineage of each sequence that has a match to this family. For each node in the resulting tree, we draw an arc in the sunburst. The radius of the arc, its distance from the root node at the centre of the sunburst, shows the taxonomic level ("superkingdom", "kingdom", etc). The length of the arc represents either the number of sequences represented at a given level, or the number of species that are found beneath the node in the tree. The weighting scheme can be changed using the sunburst controls.
In order to reduce the complexity of the representation, we reduce the number of taxonomic levels that we show. We consider only the following eight major taxonomic levels:
- superkingdom
- kingdom
- phylum
- class
- order
- family
- genus
- species
Colouring and labels
Segments of the tree are coloured approximately according to their superkingdom. For example, archeal branches are coloured with shades of orange, eukaryotes in shades of purple, etc. The colour assignments are shown under the sunburst controls. Where space allows, the name of the taxonomic level will be written on the arc itself.
As you move your mouse across the sunburst, the current node will be highlighted. In the top section of the controls panel we show a summary of the lineage of the currently highlighed node. If you pause over an arc, a tooltip will be shown, giving the name of the taxonomic level in the title and a summary of the number of sequences and species below that node in the tree.
Anomalies in the taxonomy tree
There are some situations that the sunburst tree cannot easily handle and for which we have work-arounds in place.
Missing taxonomic levels
Some species in the taxonomic tree may not have one or more of the main eight levels that we display. For example, Bos taurus is not assigned an order in the NCBI taxonomic tree. In such cases we mark the omitted level with, for example, "No order", in both the tooltip and the lineage summary.
Unmapped species names
The tree is built by looking at each sequence in the full alignment for the family. We take the name of the species given by UniProt and try to map that to the full taxonomic tree from NCBI. In some cases, the name chosen by UniProt does not map to any node in the NCBI tree, perhaps because the chosen name is listed as a synonym or a misspelling in the NCBI taxonomy.
So that these nodes are not simply omitted from the sunburst tree, we group them together in a separate branch (or segment of the sunburst tree). Since we cannot determine the lineage for these unmapped species, we show all levels between the superkingdom and the species as "uncategorised".
Since we reduce the species tree to only the eight main taxonomic levels, sequences that are mapped to the sub-species level in the tree would not normally be shown. Rather than leave out these species, we map them instead to their parent species. So, for example, for sequences belonging to one of the Vibrio cholerae sub-species in the NCBI taxonomy, we show them instead as belonging to the species Vibrio cholerae.
Too many species/sequences
For large species trees, you may see blank regions in the outer layers of the sunburst. These occur when there are large numbers of arcs to be drawn in a small space. If an arc is less than approximately one pixel wide, it will not be drawn and the space will be left blank. You may still be able to get some information about the species in that region by moving your mouse across the area, but since each arc will be very small, it will be difficult to accurately locate a particular species.
Tree controlsHide
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- Save a text representation
Selected sequences
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- graphically
- as an alignment
- sequence accessions
- sequences in FASTA format
The tree shows the occurrence of this domain across different species. More...
Species trees
We show the species tree in one of two ways. For smaller trees we try to show an interactive representation, which allows you to select specific nodes in the tree and view them as an alignment or as a set of Pfam domain graphics.
Unfortunately we have found that there are problems viewing the interactive tree when the it becomes larger than a certain limit. Furthermore, we have found that Internet Explorer can become unresponsive when viewing some trees, regardless of their size. We therefore show a text representation of the species tree when the size is above a certain limit or if you are using Internet Explorer to view the site.
If you are using IE you can still load the interactive tree by clicking the "Generate interactive tree" button, but please be aware of the potential problems that the interactive species tree can cause.
Interactive tree
For all of the domain matches in a full alignment, we count the number that are found on all sequences in the alignment. This total is shown in the purple box.
We also count the number of unique sequences on which each domain is found, which is shown in green. Note that a domain may appear multiple times on the same sequence, leading to the difference between these two numbers.
Finally, we group sequences from the same organism according to the NCBI code that is assigned by UniProt, allowing us to count the number of distinct sequences on which the domain is found. This value is shown in the pink boxes.
We use the NCBI species tree to group organisms according to their taxonomy and this forms the structure of the displayed tree. Note that in some cases the trees are too large (have too many nodes) to allow us to build an interactive tree, but in most cases you can still view the tree in a plain text, non-interactive representation. Those species which are represented in the seed alignment for this domain are highlighted.
You can use the tree controls to manipulate how the interactive tree is displayed:
- show/hide the summary boxes
- highlight species that are represented in the seed alignment
- expand/collapse the tree or expand it to a given depth
- select a sub-tree or a set of species within the tree and view them graphically or as an alignment
- save a plain text representation of the tree
Please note: for large trees this can take some time. While the tree is loading, you can safely switch away from this tab but if you browse away from the family page entirely, the tree will not be loaded.
There is 1 interaction for this family. More...
We determine these interactions using iPfam, which considers the interactions between residues in three-dimensional protein structures and maps those interactions back to Pfam families. You can find more information about the iPfam algorithm in the journal article that accompanies the website.
For those sequences which have a structure in the Protein DataBank, we use the mapping between UniProt, PDB and Pfam coordinate systems from the PDBe group, to allow us to map Pfam domains onto UniProt sequences and three-dimensional protein structures. The table below shows the structures on which the A_deamin domain has been found. There are 10 instances of this domain found in the PDB. Note that there may be multiple copies of the domain in a single PDB structure, since many structures contain multiple copies of the same protein sequence.
Loading structure mapping...


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Concept artist Christian Piccolo works at BioWare's Austin studio. Before that, he's worked on a number of cool game franchises (and other projects) like Tomb Raider, Resistance and Marvel Ultimate Alliance.
My favourite stuff, though, comes not from a game, but from a book. Piccolo managed to get a gig on DK's amazing Star Wars Complete Locations, a catalogue of my biggest and most vulnerable fetish on Earth: cutaway illustrations.
You can see more of Christian's work at his personal site.
To see the larger pics in all their glory (or so you can save them as wallpaper), right-click on them below and select "open in new tab".
Fine Art is a celebration of the work of video game artists, showcasing the best of both their professional and personal portfolios. If you're in the business and have some concept, environment or character art you'd like to share, drop us a line!


text:
dot com
Dane DeHaan photographed by Ryan McGinley, interviewed by Metallica's Lars Ulrich.
Approached Lars, with whom I'd worked before, about doing the interview, provided them with talking points, moderated the conversation, wrote text.
DANE DeHAAN IS THE MOST PROVOCATIVE YOUNG ACTOR TO HIT THE SCREEN IN YEARS. WITH DIAMETRICALLY OPPOSED ROLES THIS FALL—THE 3-D CONCERT FILM METALLICA: THROUGH THE NEVER AND THE BEAT POET BIOPIC KILL YOUR DARLINGS—HE PROVES TO BE AS TALENTED AS HE IS UNPREDICTABLE.
Dane DeHaan's exposure to Metallica began on the set of Derek Cianfrance's The Place Beyond The Pines, a film in which his character's absent father rocks a Metallica shirt for half the movie. It's maybe a perfect metaphor for Metallica's power to transcend generations, how their music resonates in your blood, ever-relevant. This year, which marks the 30th anniversary of one of the greatest debut records of all time, Kill 'Em All, the band is releasing a 3-D concert film, Metallica: Through The Never, starring the 27-year-old actor. DeHaan, who's widely considered to be a frontrunner talent among today's emergent stars, first loosed his incendiary intensity on mainstream celluloid via the award-winning HBO drama series In Treatment, but he's perhaps best known for his role in 2012's more-millenial-than-millenial superhero sleeper hitChronicle. That year also saw DeHaan working with legendary actors and filmmakers, such as Daniel Day-Lewis and Steven Spielberg (Lincoln), and Jessica Chastain, Tom Hardy, and Gary Oldman, in John Hillcoat's Nick Cave–pennedLawless. It seems inevitable that he'll become a tasteful Hollywood brand, a neo-DiCaprio vehicle starter, if not because of his unique talent then as a consequence of sheer exposure: this fall he showcases his range with two batshit opposite roles, in the aforementioned Metallica 3-D metal apocalypse sensory assault and in John Krokidas's Kill Your Darlings, a tragic story about the inner turmoil of gay lover poets in the 1940s. In Through The Never, DeHaan plays a roadie on a mission from (and through) hell, and in Darlings he plays Lucien Carr, the mostly forgotten member of a now way-too-famous group of New York writers, including a freshman from his Columbia dorm named Allen Ginsberg (played fearlessly by Daniel Radcliffe) and the two friends Carr brings to meet him, Jack Kerouac and William S. Burroughs.
Top that mercurial mélange with the fact that DeHaan just wrapped filming Sony tentpole The Amazing Spider-Man 2, rebooting the part of Harry Osborn, the role that launched a thousand Francos. Even more evidence of the lasting impression the actor leaves: This past June, at Orion Music + More, Metallica's music and arts festival, fans waiting to see an unknown band on a tiny side stage were gobsmacked when Metallica's lead singer, James Hetfield, walked up to the mic to make an introduction and suddenly the rest of Metallica rushed the stage and proceeded to play Kill 'Em All, from start to finish. The name of this fictional band impersonated by musical legends? DeHaan. Here, Dane raps out with Metallica's legendary drummer and autodidactic cinephile, Lars Ulrich, and VMAN editor, Elliott David.
LARS ULRICH So Dane. Let's talk. Are you in New York?
DANE DEHAAN Yeah. I'm in New York City.
LARS Are you doing the Spider-Man grind still?
DANE Yeah, we have one week left exactly.
LARS And how has that experience been?
DANE It's been really crazy. I've never had this much time to make a movie, which is kind of a luxury, having six months to do something. You can truly take your time to make sure you're totally ready to do the things you have to do. And it's all, just in terms of budget and production value, pretty mind-blowing at times. So I've found it's in some ways easier, because you don't have to pretend as much. The sets are amazing and they kind of just put you there.
LARS Are you doing a lot of green screen?
DANE Now we are doing more green screen, but for the most part—for the first, like, five months or so—it was actually pretty heavy acting work. What I like about Spider-Man is how human it still is. There are special effects and stuff, but the actual relationships are really strong and people's problems are real, so the acting work ends up being very fulfilling.
LARS Obviously it's the first time you've done something of this size. Where does it lie compared to some of the more independent films that you've done, in terms of the stress level of being in the moment?
DANE When making an independent movie, and you're shooting it in 24 days and it's a feature-length movie, you're shooting probably like seven plus pages a day, every single day, and you're working 14-hour days. So you have to go in ready to do that. But on Spider-Man, you're filming anywhere from an eighth of a page to three pages a day. And you've probably had a couple of weeks or a month to prepare just that specific scene. So it takes pressure off simply because there's more time to prepare.
LARS You're fairly well known for all the In Treatment stuff, and you also had a stint on True Blood. So you've done theater, you've done television and independent films, and now a super-big-budget big-studio film. Talk a little bit about the television element.
DANE In Treatment is definitely a unique television experience for an actor because those episodes are like 30 pages [of] just dialog between two people. You get the next script as soon as you're done shooting, and you probably have like five days before you shoot another 30 pages. It's very formulaic and consequently very fast-paced in nature. But when you're working with Derek [Cianfrance], all of those rules no longer exist. You show up on set and he doesn't even call action. He just kind of lets the camera roll and by the end of the day you get something. But ultimately the acting work is very similar, in terms of my job within that world. It's just about adapting to different circumstances.
LARS Are you happy to have left television or even theater behind? Or do you feel you'd like to go back to that intensity at some point?
DANE I think theater is something I'll always want to do because that's where I started. But I also feel that I spent the first 25 years of my life in theater and film is a whole new world. I like the freedom that film gives me verses the formulaic nature of television. But I guess never say never? There are exceptions to every rule, but right now I'd like to continue to capitalize on my momentum in the film industry and then go back to the theater when the time is right. When you play those different stadiums, do you find that your performances change a lot, given the size of the venue?
LARS I realize now that one of the things that keeps Metallica alive is that we always try to alter our experiences and explore environments. We'll play anything from stadiums down to backyard BBQs. When you play stadiums, you really have to project out to the people who are just little dots on the horizon, and that's the main reason we always play arenas in the round: to stay closer to a bigger portion of the audience and really feel an experience of sharing the moment. I love the smaller places because it's incredibly fulfilling to look right into the eyes of the people you're playing to. Last weekend, at our live festival [Orion Music + More, in Detroit], we played two sets: one was on the main big fuck-off stage in front of like 30,000 people, and the other was on a small side stage about the size of a hotel room under the suspicious name—I know you know this—of DeHaan. It was super intimate and just fun and old-school. So to be able to go flip around all these different experiences all the time is sort of what keeps it alive. I had Derek [Cianfrance] in my film tent at Orion last year. Talk a little more about what you said earlier, that he sometimes doesn't even yell action, he just lets you guys run with it.
DANE Derek has this amazing way of capturing real moments. If the scene is stealing prescription drugs, what he'll do is hire the guy from the counter who actually works in the Schenectady pharmacy and he won't tell him what the scene is—he'll just start rolling the camera and I'll rob the store. After the first take he'll go up to him and say, "Do you know what's going on?" And the guy will be like, "He's robbing my store," and Derek is like, "Why didn't you do anything about it?" You're really affected by a performance when somebody is actually doing something, not pretending to do something. When I act, I don't normally think about my mannerisms or that kind of thing, it comes more from finding the character within myself, it's about creating that reality inside my head and making those relationships real. And then hopefully that's what will inform the performance. When you're on set, it's really about fooling yourself into believing what's happening, and if you do your body will react appropriately. You know, Derek is the one who gave me my first Metallica album, and it was duringPines that I really listened to you guys.
LARS That's great. Derek would send me these texts, like, "I'm in a minivan with the kids and we're listening to 'Blackened' and it's 7:15 in the morning," and it just puts a big smile on my face.
ELLIOTT DAVID Lars, is Derek the one who introduced you to Dane?
LARS I see a lot of films with my kids, and we saw Chronicle when it came out. There are a lot of great actors out there, but when Dane shows up in Chronicle, there's a different kind of reality to what he brings to the character. He's at a different level than all his peers, and I don't mean that disrespectfully to his peers—it's just about Dane's intensity. So when it came time to cast Trip, just about a year ago, Dane, you were the first name that came up. So I got in touch with Derek and I said, "We are going to reach out to Dane and could you also help me reach out?" I wanted to make sure it didn't get lost between the agents and the casting directors. I wanted to get to you personally that we really feel that you are Trip, and we're going to basically lay down in front of a train until it becomes a reality. And then [Through The Never director] Nimród reached out and the whole thing just sort of ended up working out fairly effortlessly.
DANE When I got sent the script, it was this crazy story and I remember being, like, this is just so insane that I can't not read further. I'd never read anything remotely like this—it really piqued my interest, just from its pure insanity. Then I sat down with Nimród for lunch in Culver City and he had the storyboards for it and it all started to make sense. It went from this thing on first reading, like, Seriously, what the fuck? I have no idea what this is, to an epic, insane one-of-a-kind journey that really means something, especially to Nimrod. It was his passion about it—and obviously my want to be around you guys and see what it's like to be in that world—that drove me to be a part of it.
LARS In the last couple years, it's dawned on me that I get way more inspired by film then I do by music. Film makes me want to be creative and when I see a great performance or a film that's really well written, it makes me want to make music. When you see a movie like Blue Valentine [directed by Cianfrance], it makes you want to create whatever it is you create. When I see a movie like The Place Beyond the Pines, it makes me want to write songs with James Hetfield and make another Metallica record. Having your eyes open to what goes on around you and what sort of culture you gravitate toward is the stuff that inspires you.
ELLIOTT Dane, do you participate in any other artistic mediums that inspire you creatively—especially with research forKill Your Darlings, since it's a period piece about Ginsberg and the beat poets during their college years?
DANE I've always just been obsessed with acting. I like reading, but I can't play any instruments. I can sing, but I have like a third-grade drawing level, so it's always been about acting. But I'm glad you mentioned Kill Your Darlings because, Lars, what you were saying about challenging yourself and keeping it different—I honestly feel that I couldn't have two more polar opposite movies coming out in the fall, between Through the Never and Darlings. So I really hope to get some Metallica fans to go see Kill Your Darlings and get some people who saw Darlings to go to the Metallica movie.
LARS And then we are contributing to the fucking widening blurring of our culture, that's perfect.


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Fully stocked repair vans so most repairs are completed same day.
Repairs you can trust
When it comes to GE freezer repair in Escondido, not only do our highly skilled technicians use Genuine GE Appliances Parts, but they also come equipped with extensive training, product knowledge and industry insight. Whether your freezer is old or new — and no matter which GE Appliances line it belongs to — our talented technicians have it under control and will get it fixed right for you. Best yet, we're quick and competitively priced, so give us a call today!
- Courteous, highly skilled Appliance Repair Technicians
- Competitive pricing
- Fast, easy scheduling by phone or online
- Flexible appointment times
- Inexpensive extended warranties
- Genuine GE Appliances Parts