automated-analytics/bionlp2004 · Datasets at AI快站

200

Our results point to a novel alternative mechanism of action of alpha-tcp .

201

Central nervous system-derived cells express a kappa B-binding activity that enhances human immunodeficiency virus type 1 transcription in vitro and facilitates TAR -independent transactivation by Tat .

<cell_type>Central nervous system-derived cells</cell_type> express a kappa B-binding activity that enhances human immunodeficiency virus type 1 transcription in vitro and facilitates <dna>TAR</dna> -independent transactivation by <protein>Tat</protein> .

202

The Tat protein of human immunodeficiency virus type 1 ( HIV-1 ) is a potent activator of long terminal repeat -directed transcription .

The <protein>Tat protein</protein> of human immunodeficiency virus type 1 ( HIV-1 ) is a potent activator of <dna>long terminal repeat</dna> -directed transcription .

203

While in most cell types , activation requires interaction of Tat with the unusual transcription element TAR , astrocytic glial cells support TAR -independent transactivation of HIV-1 transcription by Tat .

While in most cell types , activation requires interaction of Tat with the unusual <dna>transcription element</dna> <dna>TAR</dna> , <cell_type>astrocytic glial cells</cell_type> support <dna>TAR</dna> -independent transactivation of HIV-1 transcription by Tat .

204

This alternative pathway of Tat activation is mediated by the viral enhancer , a kappa B domain capable of binding the prototypical form of the transcription factor nuclear factor kappa B ( NF-kappa B ) present in many cell types , including T lymphocytes .

This alternative pathway of <protein>Tat</protein> activation is mediated by the <dna>viral enhancer</dna> , a kappa B domain capable of binding the prototypical form of the <protein>transcription factor</protein> nuclear factor kappa B ( <protein>NF-kappa B</protein> ) present in many cell types , including <cell_type>T lymphocytes</cell_type> .

205

Tat transactivation mediated by the kappa B domain is sufficient to allow replication of TAR -deleted mutant HIV-1 in astrocytes .

<protein>Tat</protein> transactivation mediated by the <dna>kappa B domain</dna> is sufficient to allow replication of <dna>TAR</dna> -deleted mutant HIV-1 in <cell_type>astrocytes</cell_type> .

206

The present study demonstrates the existence of kappa B-specific binding factors present in human glial astrocytes that differ from prototypical NF-kappa B .

The present study demonstrates the existence of <protein>kappa B-specific binding factors</protein> present in <cell_type>human glial astrocytes</cell_type> that differ from prototypical <protein>NF-kappa B</protein> .

207

The novel astrocyte-derived kappa B-binding activity is retained on an HIV-1 Tat affinity column , while prototypical NF-kappa B from Jurkat T cells is not .

The novel astrocyte-derived kappa B-binding activity is retained on an HIV-1 <protein>Tat</protein> affinity column , while prototypical <protein>NF-kappa B</protein> from <cell_line>Jurkat T cells</cell_line> is not .

208

In vitro transcription studies demonstrate that astrocyte-derived kappa B-binding factors activate transcription of the HIV-1 long terminal repeat and that this activation is dependent on the kappa B domain .

In vitro transcription studies demonstrate that <protein>astrocyte-derived kappa B-binding factors</protein> activate transcription of the <dna>HIV-1 long terminal repeat</dna> and that this activation is dependent on the <dna>kappa B domain</dna> .

209

Moreover , TAR -independent transactivation of HIV-1 transcription is reproduced in vitro in an astrocyte factor-dependent manner which correlates with kappa B-binding activity .

Moreover , <dna>TAR</dna> -independent transactivation of HIV-1 transcription is reproduced in vitro in an astrocyte factor-dependent manner which correlates with kappa B-binding activity .

210

The importance of the central nervous system-enriched kappa B transcription factor in the regulation of HIV-1 expression is discussed .

The importance of the <protein>central nervous system-enriched kappa B</protein> <protein>transcription factor</protein> in the regulation of HIV-1 expression is discussed .

211

Human interleukin-13 activates the interleukin-4-dependent transcription factor NF-IL4 sharing a DNA binding motif with an interferon-gamma-induced nuclear binding factor .

<protein>Human interleukin-13</protein> activates the <protein>interleukin-4-dependent transcription factor</protein> <protein>NF-IL4</protein> sharing a <protein>DNA binding motif</protein> with an <protein>interferon-gamma-induced nuclear binding factor</protein> .

212

The effects of interleukin-13 ( IL-13 ) and interleukin-4 ( IL-4 ) on cellular functions were shown to be quite similar .

The effects of <protein>interleukin-13</protein> ( <protein>IL-13</protein> ) and <protein>interleukin-4</protein> ( <protein>IL-4</protein> ) on cellular functions were shown to be quite similar .

213

We provide evidence that in monocytes as well as in T lymphocytes both IL-4 and IL-13 activate the same recently identified transcription factor NF-IL4 which binds to the specific responsive element IL-4RE .

We provide evidence that in monocytes as well as in <cell_type>T lymphocytes</cell_type> both <protein>IL-4</protein> and <protein>IL-13</protein> activate the same recently identified <protein>transcription factor</protein> <protein>NF-IL4</protein> which binds to the <dna>specific responsive element IL-4RE</dna> .

214

In addition , we show that a nuclear factor activated by interferon-gamma also interacts with the IL-4RE .

In addition , we show that a <protein>nuclear factor</protein> activated by interferon-gamma also interacts with the <dna>IL-4RE</dna> .

215

It differs from NF-IL4 in the electrophoretic mobility of the complex with DNA , in its DNA-binding specificity and in the proteins interacting with the DNA sequence .

It differs from <protein>NF-IL4</protein> in the electrophoretic mobility of the complex with DNA , in its DNA-binding specificity and in the proteins interacting with the <dna>DNA sequence</dna> .

216

Sensitivity against various enzyme inhibitors suggests that components of the signal transduction pathway are shared by all three cytokines .

Sensitivity against various enzyme inhibitors suggests that components of the signal transduction pathway are shared by all three <protein>cytokines</protein> .

217

Encephalomyocarditis virus internal ribosomal entry site RNA-protein interactions .

218

Translational initiation of encephalomyocarditis virus ( EMCV ) mRNA occurs by ribosomal entry into the 5 ' nontranslated region of the EMCV mRNA , rather than by ribosomal scanning .

Translational initiation of <rna>encephalomyocarditis virus ( EMCV ) mRNA</rna> occurs by ribosomal entry into the <dna>5 ' nontranslated region</dna> of the <rna>EMCV mRNA</rna> , rather than by ribosomal scanning .

219

Internal ribosomal binding requires a cis-acting element termed the internal ribosomal entry site ( IRES ) .

Internal ribosomal binding requires a <dna>cis-acting element</dna> termed the <dna>internal ribosomal entry site</dna> ( <dna>IRES</dna> ) .

220

IRES elements have been proposed to be involved in the translation of picornavirus mRNAs and some cellular mRNAs .

<dna>IRES elements</dna> have been proposed to be involved in the translation of <rna>picornavirus mRNAs</rna> and some <rna>cellular mRNAs</rna> .

221

Internal ribosome binding likely requires the interaction of trans-acting factors that recognize both the mRNA and the ribosomal complex .

Internal ribosome binding likely requires the interaction of <protein>trans-acting factors</protein> that recognize both the <rna>mRNA</rna> and the <protein>ribosomal complex</protein> .

222

Five cellular proteins ( p52 , p57 , p70 , p72 , and p100 ) cross-link the EMCV IRES or fragments of the IRES .

Five <protein>cellular proteins</protein> ( <protein>p52</protein> , <protein>p57</protein> , <protein>p70</protein> , <protein>p72</protein> , and <protein>p100</protein> ) cross-link the EMCV <dna>IRES</dna> or fragments of the <dna>IRES</dna> .

223

For one of these proteins , p57 , binding to the IRES correlates with translation .

For one of these proteins , <protein>p57</protein> , binding to the <dna>IRES</dna> correlates with translation .

224

Recently , p57 was identified to be very similar , if not identical , to polypyrimidine tract-binding protein .

Recently , <protein>p57</protein> was identified to be very similar , if not identical , to <protein>polypyrimidine tract-binding protein</protein> .

225

On the basis of cross-linking results with 21 different EMCV IRES fragments and cytoplasmic HeLa extract or rabbit reticulocyte lysate as the source of polypeptides , consensus binding sites for p52 , p57 , p70 , and p100 are proposed .

On the basis of cross-linking results with 21 different <dna>EMCV IRES fragments</dna> and cytoplasmic HeLa extract or rabbit reticulocyte lysate as the source of polypeptides , <dna>consensus binding sites</dna> for <protein>p52</protein> , <protein>p57</protein> , <protein>p70</protein> , and <protein>p100</protein> are proposed .

226

It is suggested that each of these proteins recognizes primarily a structural feature of the RNA rather than a specific sequence .

227

A novel heterodimerization partner for thyroid hormone receptor .

A novel <protein>heterodimerization partner</protein> for <protein>thyroid hormone receptor</protein> .

228

Peroxisome proliferator-activated receptor .

<protein>Peroxisome proliferator-activated receptor</protein> .

229

Retinoid-like receptors play a central role in hormonal responses by forming heterodimers with other nuclear hormone receptors .

<protein>Retinoid-like receptors</protein> play a central role in hormonal responses by forming <protein>heterodimers</protein> with other <protein>nuclear hormone receptors</protein> .

230

In this study we have identified the peroxisome proliferator-activated receptor ( PPAR ) as a new thyroid hormone receptor ( THR ) auxiliary nuclear protein , heterodimerizing with THR in solution .

In this study we have identified the <protein>peroxisome proliferator-activated receptor</protein> ( <protein>PPAR</protein> ) as a new <protein>thyroid hormone receptor ( THR ) auxiliary nuclear protein</protein> , heterodimerizing with <protein>THR</protein> in solution .

231

Although these heterodimers do not recognize a classical thyroid hormone response element ( TRE ) characterized by direct repeat separated by four nucleotides ( DR+4 ) , PPAR behaves as a dominant negative regulator of thyroid hormone ( TH ) action .

Although these <protein>heterodimers</protein> do not recognize a classical <dna>thyroid hormone response element</dna> ( <dna>TRE</dna> ) characterized by direct repeat separated by four nucleotides ( <dna>DR+4</dna> ) , <protein>PPAR</protein> behaves as a dominant negative regulator of thyroid hormone ( TH ) action .

232

However , a TH-dependent positive effect is elicited by selective interaction of the THR beta-PPAR but not the THR alpha-PPAR heterodimer with a novel TRE ( DR+2 ) .

However , a TH-dependent positive effect is elicited by selective interaction of the <protein>THR beta-PPAR</protein> but not the <protein>THR alpha-PPAR heterodimer</protein> with a novel <dna>TRE</dna> ( <dna>DR+2</dna> ) .

233

The critical region of THR beta was mapped to 3 amino acids in the distal box of the DNA binding domain .

The critical region of <protein>THR</protein> beta was mapped to 3 amino acids in the <protein>distal box</protein> of the <protein>DNA binding domain</protein> .

234

Hence , PPAR can positively or negatively influence TH action depending on TRE structure and THR isotype .

Hence , <protein>PPAR</protein> can positively or negatively influence TH action depending on <dna>TRE</dna> structure and <protein>THR isotype</protein> .

235

Comparison of retinoic acid and phorbol myristate acetate as inducers of monocytic differentiation .

236

Several human myeloid leukemia cell lines growing in vitro can be induced to differentiate to more mature monocyte/macrophage-like cells by treatment with protein kinase C -activating phorbol esters , such as PMA .

Several <cell_line>human myeloid leukemia cell lines</cell_line> growing in vitro can be induced to differentiate to more mature <cell_type>monocyte/macrophage-like cells</cell_type> by treatment with <protein>protein kinase C</protein> -activating phorbol esters , such as PMA .

237

In addition to PMA , cells of the THP-1 myeloid leukemia cell line acquire macrophage-like characteristics after treatment with all-trans retinoic acid ( RA ) .

In addition to PMA , cells of the <cell_line>THP-1 myeloid leukemia cell line</cell_line> acquire macrophage-like characteristics after treatment with all-trans retinoic acid ( RA ) .

238

To analyze the signal transduction mechanisms induced by RA , we first compared the effects of PMA and RA on the expression of genes which are known to be regulated during monocytic differentiation .

239

Both RA and PMA effectively down-regulated c-myc expression , while c-myb expression decreased only after PMA treatment .

Both RA and PMA effectively down-regulated <dna>c-myc</dna> expression , while <dna>c-myb</dna> expression decreased only after PMA treatment .

240

Expression of the beta 2-integrin genes , CD11a and CD11b , was clearly increased after both of these treatments .

Expression of the <dna>beta 2-integrin genes</dna> , <dna>CD11a</dna> and <dna>CD11b</dna> , was clearly increased after both of these treatments .

241

Their effects on the src-family tyrosine kinase genes were different : hck expression was similarly induced by these agents but lyn expression was stronger and more rapid after RA treatment .

Their effects on the <dna>src-family tyrosine kinase genes</dna> were different : <dna>hck</dna> expression was similarly induced by these agents but lyn expression was stronger and more rapid after RA treatment .

242

RA also enhanced lyn mRNA production rapidly in HL-60 , indicating that the activation of lyn gene expression is common in monocytic and granulocytic maturation of myeloid leukemia cells .

RA also enhanced <rna>lyn mRNA</rna> production rapidly in <cell_line>HL-60</cell_line> , indicating that the activation of <dna>lyn gene</dna> expression is common in monocytic and granulocytic maturation of <cell_type>myeloid leukemia cells</cell_type> .

243

To examine whether the AP-1 enhancer activity is involved in RA-induced monocytic differentiation , THP-1 cells were transiently transfected with a chloramphenicol acetyl transferase ( CAT ) -reporter gene containing 5 copies of the AP-1 binding sites .

To examine whether the <dna>AP-1 enhancer</dna> activity is involved in RA-induced monocytic differentiation , <cell_line>THP-1 cells</cell_line> were transiently transfected with a <dna>chloramphenicol acetyl transferase ( CAT ) -reporter gene</dna> containing 5 copies of the <dna>AP-1 binding sites</dna> .

244

In contrast to PMA , RA did not induce any CAT activity in these cells , thus suggesting that the RA-induced changes in the expression of those genes described above were not dependent on the AP-1 enhancer activity .

In contrast to PMA , RA did not induce any <protein>CAT</protein> activity in these cells , thus suggesting that the RA-induced changes in the expression of those genes described above were not dependent on the <dna>AP-1 enhancer</dna> activity .

245

An active v-abl protein tyrosine kinase blocks immunoglobulin light-chain gene rearrangement .

An active <protein>v-abl protein tyrosine kinase</protein> blocks <dna>immunoglobulin light-chain gene</dna> rearrangement .

246

Lymphoid cells transformed by Abelson murine leukemia virus have provided one of the classic models for study of early B-cell development and immunoglobulin rearrangement .

<cell_type>Lymphoid cells</cell_type> transformed by Abelson murine leukemia virus have provided one of the classic models for study of early B-cell development and <protein>immunoglobulin</protein> rearrangement .

247

Most of these cells have rearranged their heavy-chain locus but not their light chain genes , suggesting that an active v-abl protein interferes with this differentiation step .

Most of these cells have rearranged their <dna>heavy-chain locus</dna> but not their <dna>light chain genes</dna> , suggesting that an active <protein>v-abl protein</protein> interferes with this differentiation step .

248

To test this hypothesis , light-chain gene structure was examined in pre-B cells transformed by temperature-sensitive mutants of the Abelson virus and in derivatives that survive at the nonpermissive temperature because they express a human BCL-2 gene .

To test this hypothesis , <dna>light-chain gene structure</dna> was examined in <cell_line>pre-B cells</cell_line> transformed by temperature-sensitive mutants of the Abelson virus and in derivatives that survive at the nonpermissive temperature because they express a <dna>human BCL-2 gene</dna> .

249

Our studies reveal that inactivation of the v-abl protein tyrosine kinase triggers high-frequency rearrangement of kappa and lambda light-chain genes .

Our studies reveal that inactivation of the <protein>v-abl protein tyrosine kinase</protein> triggers high-frequency rearrangement of <dna>kappa and lambda light-chain genes</dna> .

250

These events are accompanied by marked increases in the expression of RAG-1 and RAG-2 RNAs .

These events are accompanied by marked increases in the expression of <rna>RAG-1 and RAG-2 RNAs</rna> .

251

These increases occur in the absence of protein synthesis but are dependent on inactivation of the v-abl protein tyrosine kinase .

These increases occur in the absence of protein synthesis but are dependent on inactivation of the <protein>v-abl protein tyrosine kinase</protein> .

252

As documented in the accompanying paper ( Klug et al. , this issue ) , an active v-abl protein also suppresses the activity of NF-kappa B/rel and expression controlled by the kappa intron enhancer .

As documented in the accompanying paper ( Klug et al. , this issue ) , an active <protein>v-abl protein</protein> also suppresses the activity of <protein>NF-kappa B/rel</protein> and expression controlled by the <dna>kappa intron enhancer</dna> .

253

Together these data demonstrate that the v-abl protein specifically interferes with light-chain gene rearrangement by suppressing at least two pathways essential for this stage of B-cell differentiation and suggest that tyrosine phosphorylation is important in regulating RAG gene expression .

Together these data demonstrate that the <protein>v-abl protein</protein> specifically interferes with <dna>light-chain gene</dna> rearrangement by suppressing at least two pathways essential for this stage of <cell_type>B-cell</cell_type> differentiation and suggest that tyrosine phosphorylation is important in regulating <dna>RAG gene</dna> expression .

254

Calcium signalling in T cells stimulated by a cyclophilin B-binding protein .

Calcium signalling in <cell_type>T cells</cell_type> stimulated by a <protein>cyclophilin B-binding protein</protein> .

255

The immunosuppressant drug cyclosporin A blocks a calcium-dependent signal from the T-cell receptor ( TCR ) that normally leads to T-cell activation .

The immunosuppressant drug cyclosporin A blocks a calcium-dependent signal from the <protein>T-cell receptor</protein> ( <protein>TCR</protein> ) that normally leads to T-cell activation .

256

When bound to cyclophilin , cyclosporin A binds and inactivates the key signalling intermediate calcineurin .

When bound to <protein>cyclophilin</protein> , cyclosporin A binds and inactivates the key signalling intermediate <protein>calcineurin</protein> .

257

To identify potential cellular homologues of cyclosporin A that might regulate calcium signalling , we have cloned human genes encoding cyclophilin B-binding-proteins using the yeast two-hybrid system .

To identify potential cellular homologues of cyclosporin A that might regulate calcium signalling , we have cloned human genes encoding <protein>cyclophilin B-binding-proteins</protein> using the yeast two-hybrid system .

258

One gene product , when overexpressed in Jurkat T cells , specifically induced transcription from the interleukin-2 enhancer , by activating the T-cell-specific transcription factors NF-AT and NF-IL2A .

One gene product , when overexpressed in <cell_line>Jurkat T cells</cell_line> , specifically induced transcription from the <dna>interleukin-2 enhancer</dna> , by activating the <protein>T-cell-specific transcription factors</protein> <protein>NF-AT</protein> and <protein>NF-IL2A</protein> .

259

This protein , termed calcium-signal modulating cyclophilin ligand ( CAML ) , acts downstream of the TCR and upstream of calcineurin by causing an influx of calcium .

This protein , termed <protein>calcium-signal modulating cyclophilin ligand</protein> ( <protein>CAML</protein> ) , acts downstream of the <protein>TCR</protein> and upstream of <protein>calcineurin</protein> by causing an influx of calcium .

260

CAML appears to be a new participant in the calcium-signal transduction pathway , implicating cyclophilin B in calcium signalling , even in the absence of cyclosporin .

<protein>CAML</protein> appears to be a new participant in the calcium-signal transduction pathway , implicating <protein>cyclophilin B</protein> in calcium signalling , even in the absence of cyclosporin .

261

Expression and genomic configuration of GM-CSF , IL-3 , M-CSF receptor ( C-FMS ) , early growth response gene-1 ( EGR-1 ) and M-CSF genes in primary myelodysplastic syndromes .

Expression and genomic configuration of <protein>GM-CSF</protein> , <protein>IL-3</protein> , <protein>M-CSF receptor</protein> ( <protein>C-FMS</protein> ) , <dna>early growth response gene-1</dna> ( <dna>EGR-1</dna> ) and <dna>M-CSF genes</dna> in primary myelodysplastic syndromes .

262

Peripheral blood mononuclear cells from seventeen patients with primary myelodysplastic syndromes ( MDS ) in advanced stage were enriched for blasts and tested for ( 1 ) karyotype , ( 2 ) genomic configuration and ( 3 ) expression of IL-3 , GM-CSF , FMS and EGR-1 genes which are all located on the long arm of chromosome 5 .

Peripheral blood mononuclear cells from seventeen patients with primary myelodysplastic syndromes ( MDS ) in advanced stage were enriched for <cell_type>blasts</cell_type> and tested for ( 1 ) karyotype , ( 2 ) genomic configuration and ( 3 ) expression of <dna>IL-3 , GM-CSF , FMS and EGR-1 genes</dna> which are all located on the <dna>long arm of chromosome 5</dna> .

263

The expression of the M-CSF gene , that has been recently reassigned to the short arm of chromosome 1 ( lp ) , was also investigated .

The expression of the <dna>M-CSF gene</dna> , that has been recently reassigned to the <dna>short arm of chromosome 1</dna> ( <dna>lp</dna> ) , was also investigated .

264

Aims of the study were to ( 1 ) assess the potential role of the expression of these genes in the maintenance and expansion of the neoplastic clones and ( 2 ) search for constitutional losses or rearrangements of one allele followed by a deletion of the second allele of the same genes in the leukemic cells .

Aims of the study were to ( 1 ) assess the potential role of the expression of these genes in the maintenance and expansion of the <cell_line>neoplastic clones</cell_line> and ( 2 ) search for constitutional losses or rearrangements of one <dna>allele</dna> followed by a deletion of the second <dna>allele</dna> of the same genes in the <cell_type>leukemic cells</cell_type> .

265

The latter issue was investigated by comparing , in 8 cases , constitutive DNA from skin fibroblasts with leukemic DNA .

The latter issue was investigated by comparing , in 8 cases , <dna>constitutive DNA</dna> from <cell_type>skin fibroblasts</cell_type> with <dna>leukemic DNA</dna> .

266

Eleven of the 17 patients had abnormal karyotypes .

267

The M-CSF gene was expressed in 6 cases and the FMS and the EGR-1 genes were expressed in 2 of the latter cases .

The <dna>M-CSF gene</dna> was expressed in 6 cases and the <dna>FMS</dna> and the <dna>EGR-1 genes</dna> were expressed in 2 of the latter cases .

268

An autocrine mechanism of growth could be hypothesized only for the 2 patients whose cells expressed both the M-CSF and FMS genes .

An autocrine mechanism of growth could be hypothesized only for the 2 patients whose cells expressed both the <dna>M-CSF and FMS genes</dna> .

269

No germline changes or rearrangements were observed in any of the genes studied .

270

Thus , deregulation of genes encoding for certain hemopoietic growth factors or receptors does not seem to represent a major mechanism of MDS progression .

Thus , deregulation of genes encoding for certain <protein>hemopoietic growth factors</protein> or receptors does not seem to represent a major mechanism of MDS progression .

271

A novel human homeobox gene distantly related to proboscipedia is expressed in lymphoid and pancreatic tissues .

A novel <dna>human homeobox gene</dna> distantly related to <dna>proboscipedia</dna> is expressed in lymphoid and pancreatic tissues .

272

A novel human homeobox gene , HB9 , was isolated from a cDNA library prepared from in vitro stimulated human tonsil B lymphocytes and from a human genomic library .

A novel <dna>human homeobox gene</dna> , <dna>HB9</dna> , was isolated from a <dna>cDNA library</dna> prepared from in <cell_type>vitro stimulated human tonsil B lymphocytes</cell_type> and from a <dna>human genomic library</dna> .

273

The HB9 gene is composed of 3 exons spread over 6 kilobases of DNA .

The <dna>HB9 gene</dna> is composed of 3 <dna>exons</dna> spread over 6 kilobases of DNA .

274

An open reading frame of 1206 nucleotides is in frame with a diverged homeodomain .

An <dna>open reading frame</dna> of 1206 nucleotides is in frame with a <dna>diverged homeodomain</dna> .

275

The predicted HB9 protein has a molecular mass of 41 kilodaltons and is enriched for alanine , glycine , and leucine .

The predicted <protein>HB9 protein</protein> has a molecular mass of 41 kilodaltons and is enriched for alanine , glycine , and leucine .

276

The HB9 homeodomain is most similar to that of the Drosophila melanogaster homeobox gene proboscipedia .

The <dna>HB9 homeodomain</dna> is most similar to that of the <dna>Drosophila melanogaster homeobox gene</dna> <dna>proboscipedia</dna> .

277

Northern blot analysis of poly ( A ) RNA purified from the human B cell line RPMI 8226 and from activated T cells revealed a major mRNA transcript of 2.2 kilobases .

Northern blot analysis of <rna>poly ( A ) RNA</rna> purified from the <cell_line>human B cell line RPMI 8226</cell_line> and from <cell_type>activated T cells</cell_type> revealed a <rna>major mRNA transcript</rna> of 2.2 kilobases .

278

Similar analysis of poly ( A ) RNA from a variety of adult tissues demonstrated HB9 transcripts in pancreas , small intestine , and colon .

Similar analysis of <rna>poly ( A ) RNA</rna> from a variety of adult tissues demonstrated <dna>HB9</dna> transcripts in pancreas , small intestine , and colon .

279

Reverse transcriptase-polymerase chain reaction was used to examine HB9 RNA transcripts in hematopoietic cell lines .

Reverse transcriptase-polymerase chain reaction was used to examine <rna>HB9 RNA transcripts</rna> in <cell_line>hematopoietic cell lines</cell_line> .

280

HB9 RNA transcripts were most prevalent in several human B cell lines and K562 cells .

<rna>HB9 RNA transcripts</rna> were most prevalent in several <cell_line>human B cell lines</cell_line> and <cell_line>K562 cells</cell_line> .

281

In addition , transcripts were detected in RNA prepared from tonsil B cells and in situ hybridization studies localized them in the germinal center region of adult tonsil .

In addition , transcripts were detected in RNA prepared from <cell_type>tonsil B cells</cell_type> and in situ hybridization studies localized them in the germinal center region of adult tonsil .

282

These findings suggest the involvement of HB9 in regulating gene transcription in lymphoid and pancreatic tissues .

These findings suggest the involvement of <dna>HB9</dna> in regulating gene transcription in lymphoid and pancreatic tissues .

283

Human immunodeficiency virus type 1 Tat upregulates interleukin-2 secretion in activated T cells .

<protein>Human immunodeficiency virus type 1 Tat</protein> upregulates <protein>interleukin-2</protein> secretion in <cell_type>activated T cells</cell_type> .

284

Dysregulation of cytokines secreted by T cells may play an important role in the pathogenesis of AIDS .

Dysregulation of <protein>cytokines</protein> secreted by <cell_type>T cells</cell_type> may play an important role in the pathogenesis of AIDS .

285

To investigate the effects of human immunodeficiency virus type 1 ( HIV-1 ) Tat on interleukin-2 ( IL-2 ) expression , we used IL-2 promoter-chloramphenicol acetyltransferase constructs and IL-2-secreting Jurkat T cells as a model system .

To investigate the effects of <protein>human immunodeficiency virus type 1 ( HIV-1 ) Tat</protein> on <protein>interleukin-2</protein> ( <protein>IL-2</protein> ) expression , we used <dna>IL-2 promoter-chloramphenicol acetyltransferase constructs</dna> and <cell_line>IL-2-secreting Jurkat T cells</cell_line> as a model system .

286

Transient expression of HIV-1 Tat induced a five- to eightfold increase in IL-2 promoter activity in Jurkat T cells stimulated with phytohemagglutinin and phorbol myristate acetate .

Transient expression of <protein>HIV-1 Tat</protein> induced a five- to eightfold increase in <dna>IL-2 promoter</dna> activity in <cell_line>Jurkat T cells</cell_line> stimulated with <protein>phytohemagglutinin</protein> and phorbol myristate acetate .

287

IL-2 secretion was increased more than twofold in both Jurkat T cells and primary T cells stimulated by extracellular HIV-1 Tat protein .

<protein>IL-2</protein> secretion was increased more than twofold in both <cell_line>Jurkat T cells</cell_line> and <cell_line>primary T cells</cell_line> stimulated by <protein>extracellular HIV-1 Tat protein</protein> .

288

Analysis of mRNA suggested that Tat exerts its effect on IL-2 primarily at the transcriptional level .

Analysis of <rna>mRNA</rna> suggested that Tat exerts its effect on <protein>IL-2</protein> primarily at the transcriptional level .

289

The NF-kappa B site at positions -206 to -195 of the IL-2 promoter was required but not sufficient for the Tat effect .

The <dna>NF-kappa B site</dna> at positions <dna>-206 to -195</dna> of the <dna>IL-2 promoter</dna> was required but not sufficient for the <protein>Tat</protein> effect .

290

The Tat -mediated increase in IL-2 promoter activity could selectively be blocked by antisense tat or-unlike the analogous effect of human T-cell lymphotropic virus type 1 Tax -by cyclosporin A .

The <protein>Tat</protein> -mediated increase in <dna>IL-2 promoter</dna> activity could selectively be blocked by antisense tat or-unlike the analogous effect of <protein>human T-cell lymphotropic virus type 1 Tax</protein> -by cyclosporin A .

291

The observed increase in IL-2 levels might facilitate virus spread from or to T cells .

The observed increase in <protein>IL-2</protein> levels might facilitate virus spread from or to <cell_type>T cells</cell_type> .

292

Furthermore , it might contribute to the hypergammaglobulinemia or , together with other cytokines found to be dysregulated , the T-helper cell dysfunctions observed in AIDS patients .

Furthermore , it might contribute to the hypergammaglobulinemia or , together with other <protein>cytokines</protein> found to be dysregulated , the T-helper cell dysfunctions observed in AIDS patients .

293

Activation of nuclear factor kappa B in human lymphoblastoid cells by low-dose ionizing radiation .

Activation of <protein>nuclear factor kappa B</protein> in <cell_type>human lymphoblastoid cells</cell_type> by low-dose ionizing radiation .

294

Nuclear factor kappa B ( NF-kappa B ) is a pleiotropic transcription factor which is involved in the transcriptional regulation of several specific genes .

<protein>Nuclear factor kappa B</protein> ( <protein>NF-kappa B</protein> ) is a <protein>pleiotropic transcription factor</protein> which is involved in the transcriptional regulation of several specific genes .

295

Recent reports demonstrated that ionizing radiation in the dose range of 2-50 Gy results in expression of NF-kappa B in human KG-1 myeloid leukemia cells and human B-lymphocyte precursor cells ; the precise mechanism involved and the significance are not yet known .

Recent reports demonstrated that ionizing radiation in the dose range of 2-50 Gy results in expression of <protein>NF-kappa B</protein> in <cell_line>human KG-1 myeloid leukemia cells</cell_line> and <cell_type>human B-lymphocyte precursor cells</cell_type> ; the precise mechanism involved and the significance are not yet known .

296

The present report demonstrates that even lower doses of ionizing radiation , 0.25-2.0 Gy , are capable of inducing expression of NF-kappa B in EBV-transformed 244B human lymphoblastoid cells .

The present report demonstrates that even lower doses of ionizing radiation , 0.25-2.0 Gy , are capable of inducing expression of <protein>NF-kappa B</protein> in <cell_line>EBV-transformed 244B human lymphoblastoid cells</cell_line> .

297

These results are in a dose range where the viability of the cells remains very high .

298

After exposure to 137Cs gamma rays at a dose rate of 1.17 Gy/min , a maximum in expression of NF-kappa B was seen at 8 h after a 0.5-Gy exposure .

After exposure to 137Cs gamma rays at a dose rate of 1.17 Gy/min , a maximum in expression of <protein>NF-kappa B</protein> was seen at 8 h after a 0.5-Gy exposure .

299

Time-course studies revealed a biphasic time-dependent expression after 0.5- , 1- and 2-Gy exposures .