Mutations in NOTCH3 are the cause of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a hereditary angiopathy causing stroke and vascular dementia. All CADASIL mutations identified so far result in the loss or gain of one cysteine residue within epidermal growth factor (EGF)-like repeat domains. Here an in-frame deletion causing a loss of three cysteine residues within EGF repeat 6 is reported. These data are consistent with the hypothesis that the change toward an odd number of cysteine residues within a given EGF repeat and therefore an unpaired, reactive cysteine residue is the common and critical molecular event in CADASIL.
Mutations in NOTCH3 are the cause of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy ( CADASIL ) , a hereditary angiopathy causing stroke and vascular dementia . All CADASIL mutations identified so far result in the loss or gain of one cysteine residue within epidermal growth factor ( EGF)-like repeat domains . Here an in - frame deletion causing a loss of three cysteine residues within EGF repeat 6 is reported . These data are consistent with the hypothesis that the change toward an odd number of cysteine residues within a given EGF repeat and therefore an unpaired , reactive cysteine residue is the common and critical molecular event in CADASIL .
Which amino acid residue appears mutated in most of the cases reported with  cadasil syndrome?
Which amino acid residue appears mutated in most of the cases reported with cadasil syndrome ?
Cysteine
Cysteine