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Publication : Protein kinase C δ (PKCδ) splice variants modulate apoptosis pathway in 3T3L1 cells during adipogenesis: identification of PKCδII inhibitor.

First Author  Patel R Year  2013
Journal  J Biol Chem Volume  288
Issue  37 Pages  26834-46
PubMed ID  23902767 Mgi Jnum  J:203531
Mgi Id  MGI:5527210 Doi  10.1074/jbc.M113.482638
Citation  Patel R, et al. (2013) Protein kinase C delta (PKCdelta) splice variants modulate apoptosis pathway in 3T3L1 cells during adipogenesis: identification of PKCdeltaII inhibitor. J Biol Chem 288(37):26834-46
abstractText  Increased food intake and lack of physical activity results in excess energy stored in adipocytes, and this imbalance contributes to obesity. New adipocytes are required for storage of energy in the white adipose tissue. This process of adipogenesis is widely studied in differentiating 3T3L1 preadipocytes in vitro. We have identified a key signaling kinase, protein kinase C delta (PKCdelta), whose alternative splice variant expression is modulated during adipogenesis. We demonstrate that PKCdeltaII splice variant promotes survival in differentiating 3T3L1 cells through the Bcl2 pathway. Here we demonstrate that resveratrol, a naturally occurring polyphenol, increases apoptosis and inhibits adipogenesis along with disruption of PKCdelta alternative splicing during 3T3L1 differentiation. Importantly, we have identified a PKCdeltaII splice variant inhibitor. This inhibitor may be a valuable tool with therapeutic implications in obesity.
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