The increase in BIK expression following ERK1/2 pathway inhibition is a consequence of G₁ cell-cycle arrest and not a direct effect on BIK protein stability

BIK (BCL2-interacting killer) is a pro-apoptotic BH3 (BCL2 homology domain 3)-only protein and a member of the BCL2 protein family. It was proposed recently that BIK abundance is controlled by ERK1/2 (extracellular-signal-regulated kinase 1/2)-catalysed phosphorylation, which targets the protein for...

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Bibliographic Details
Published inBiochemical journal Vol. 459; no. 3; p. 513
Main Authors Sale, Matthew J, Cook, Simon J
Format Journal Article
LanguageEnglish
Published England 01.05.2014
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