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BAD Phosphorylation

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The ability of multicellular organisms to maintain cellular homeostasis is critically dependent on a balance between cell survival and cell death (apoptosis). The responsiveness of individual cells to death signals varies greatly depending on the presence of continuous survival cues from the extracellular environment. The perturbation of normal cell survival mechanisms, leading to an increase in cell survival or cell death plays an important role in the development of a number of disease states, including cancer. BAD (BCL2 Associated Death Promoter) is a pro-apoptotic critical regulatory component of the intrinsic cell death machinery that exerts its death-promoting effect upon heterodimerization with the antiapoptotic proteins of the BCL2 family defined by conserved regions of identity called BH (BCL2 homology) domains (Ref.1).

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1.BAD Ser128 Is Not Phosphorylated by c-Jun NH2-Terminal Kinase for Promoting Apoptosis.
Zhang J, Liu J, Yu C, Lin A.
Cancer Res. 2005 Sep 15;65(18):8372-8.
2.Caspase cleavage enhances the apoptosis-inducing effects of BAD.
Condorelli F, Salomoni P, Cotteret S, Cesi V, Srinivasula SM, Alnemri ES, Calabretta B.
Mol Cell Biol. 2001 May; 21(9): 3025-36.
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