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PKB/Akt

a key mediator of cell proliferation, survival and insulin responses?

MRC Protein Phosphorylation Unit, Department of Life Sciences, University of Dundee, Dundee DD1 5EH, UK
^* Author for correspondence (e-mail: d.r.alessi{at}dundee.ac.uk )

View larger version (21K): [in a new window]   Fig. 1. The mechanisms by which PKB may regulate the cell cycle, apoptosis and insulin signalling. Only the substrates that have been proposed to be directly phosphorylated by PKB and discussed in the main text are shown. PKB may also promote cell survival by phosphorylating I-B kinase-, the breast cancer susceptibility gene 1, human telomerase reverse transcriptase, the GTPases Rac1/CDC42 and the serine/threonine protein kinase Raf1, but the roles that these phosphorylations play are controversial and require further investigation. Note that, because of the limitations in the experimental approaches that are being to dissect the PKB pathway, some of the proposed substrates for PKB may ultimately turn out not to be phosphorylated physiologically by PKB but by other protein kinases instead. Abreviations: FKHR, forkhead transcription factor; 6-PF2-K, cardiac isoform of heart 6-phosphofructo-2-kinase; GSK3, glycogen synthase kinase 3; eNOS, endothelial nitric oxide synthase; PDE-3B, phosphodiesterase 3B; Ask1, apoptosis signal-regulating kinase 1.