Abstract:
:Human type 2 diabetes is associated with β-cell apoptosis, and human islets from diabetic donors are ∼80% deficient in PAK1 protein. Toward addressing linkage of PAK1 to β-cell survival, PAK1-siRNA targeted MIN6 pancreatic β-cells were found to exhibit increased caspase-3 cleavage, cytosolic cytochrome-C and the pro-apoptotic protein Bad. PAK1(+/-) heterozygous mouse islets recapitulated the upregulation of Bad protein expression, as did hyperglycemic treatment of human or mouse islets; Bad levels were exacerbated most in PAK1(+/-) islets subjected to hyperglycemic stress. These data implicate PAK1 in β-cell survival via quenching of Bad protein expression, and suggest PAK1 as potential molecular target to preserve β-cell mass.
journal_name
FEBS Open Biojournal_title
FEBS open bioauthors
Wang Z,Thurmond DCdoi
10.1016/j.fob.2012.09.001subject
Has Abstractpub_date
2012-09-08 00:00:00pages
273-7issn
2211-5463pii
FOB47journal_volume
2pub_type
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