Title : Opposing actions of insulin and arsenite converge on PKCdelta to alter keratinocyte proliferative potential and differentiation.

Pub. Date : 2010 Apr

PMID : 20082316






4 Functional Relationships(s)
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1 In present work, we show that insulin signaling, probably through the IGF-I receptor, is required for the increase in cell size accompanying differentiation and that this is opposed by arsenite. arsenite insulin Homo sapiens
2 We further examine the impact of insulin and arsenite on PKCdelta, a known key regulator of keratinocyte differentiation, and show that insulin increases the amount, tyrosine phosphorylation, and membrane localization of PKCdelta. arsenite insulin Homo sapiens
3 All these effects are prevented by exposure of cells to arsenite or to inhibitors of downstream effectors of insulin (phosphotidylinositol 3-kinase and mammalian target of rapamycin). arsenite insulin Homo sapiens
4 Finally, inhibiting epidermal growth factor receptor kinase activity diminished the ability of arsenite to prevent cell enlargement and to suppress insulin-dependent PKCdelta amount and tyrosine 311 phosphorylation. arsenite insulin Homo sapiens