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• W2088955963 abstract "Abstract The Bcl-2 protein is one of the key components of biochemical pathways controlling programmed cell death. The function of this protein can be regulated by posttranslational modifications. Phosphorylation of Bcl-2 has been considered to be significantly associated with cell cycle arrest in the G2/M phase of the cell cycle, and with cell death caused by defects of microtubule dynamics. This study shows that phosphorylation of Bcl-2 can be induced by heavy metals due to activation of the Jun N-terminal kinase pathway that is not linked to the G2/M cell cycle arrest. Furthermore, we demonstrate that hyperphosphorylated Bcl-2 protein is a more potent inhibitor of zinc-induced cell death than its hypophosphorylated mutant form. These data suggest that regulation of Bcl-2 protein function by phosphorylation is an important part of cell responses to stress." @default.
• W2088955963 created "2016-06-24" @default.
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• W2088955963 date "2008-11-13" @default.
• W2088955963 modified "2023-10-17" @default.
• W2088955963 title "Heavy metals induce phosphorylation of the Bcl-2 protein by Jun N-terminal kinase" @default.
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• W2088955963 doi "https://doi.org/10.1515/bc.2009.007" @default.
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