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Physicochemical compatibility

Phosphorylation of S136 in Bcl2 antagonist of cell death (Bad) by RAC-alpha serine/threonine-protein kinase (Akt1) in response to survival and growth signals such as Interleukin-3 (Il3) induces binding to 14-3-3 protein theta (Ywhaq). Binding of 14-3-3 protein theta (Ywhaq) results in dissociation of Bcl2 antagonist of cell death (Bad) from Bcl-2-like protein 1 (Bcl2l1), and thereby inhibits the pro-apoptotic activity of Bcl2 antagonist of cell death (Bad) by allowing liberated Bcl-2-like protein 1 (Bcl2l1) to exert its anti-apoptotic effect on pro-apoptotic proteins like Apoptosis regulator BAX (Bax).

(1) Bcl2 antagonist of cell death (Bad)
(2) 14-3-3 protein theta (Ywhaq)


(1) Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L)
Zha et al. Cell (1996)

(2) Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery.
Datta et al. Cell (1997)

(3) How BAD phosphorylation is good for survival.
et al. Nat. Cell Biol. (1999)

(4) 14-3-3 proteins and survival kinases cooperate to inactivate BAD by BH3 domain phosphorylation.
Datta et al. Mol. Cell (2000)

See also

Other switches involving interfaces
14-3-3 protein - 38 more (view)
LIG_14-3-3_1 - 13 more (view)

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