Phosphorylation of the pro-apoptotic protein BAD on serine 155, a novel site, contributes to cell survival

Current Biology

Volumn 10, Issue 18, 2000, Pages 1151-1154

  Virdee, K ^a   Parone, P A ^a   Tolkovsky, A M ^a  

^a UNIVERSITY OF CAMBRIDGE   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

EID: 0034699352     PISSN: 09609822     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0960-9822(00)00702-8     Document Type: Article

References (20)

1. The Kit receptor promotes cell survival via activation of PI 3-kinase and subsequent Akt-mediated phosphorylation of Bad on Ser136
2. Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery
3. Interleukin-3-induced phosphorylation of Bad through the protein kinase Akt
4. BAD, a heterodimeric partner for bcl-x(l) and bcl-2, displaces bax and promotes cell-death
5. Serine phosphorylation of death agonist BAD in response to survival factors results in binding to 14-3-3 not BCL-XL
6. Phosphorylation and inactivation of BAD by mitochondria-anchored protein kinase A
7. Cell survival promoted by the Ras-MAPK signaling pathway by transcription-dependent and -independent mechanisms
8. Regulation of BAD phosphorylation at serine 112 by the Ras-mitogen-activated protein kinase pathway
9. Rsk1 mediates a MEK-MAP kinase cell survival signal
10. p21-activated kinase 1 phosphorylates the death agonist Bad and protects cells from apoptosis
11. Dissociation of cytokine-induced phosphorylation of Bad and activation of PKB/akt: Involvement of MEK upstream of Bad phosphorylation
12. Regulation of Bad phosphorylation and association with Bcl XL by the MAPK/Erk kinase
13. Activation of mitochondrial Raf-1 is involved in the antiapoptotic effects of Akt
14. Expression of constitutively active Raf-1 in the mitochondria restores antiapoptotic and leukemogenic potential of a transformation-deficient BCR/ABL mutant
15. Bcl-2 targets the protein kinase Raf-1 to mitochondria
16. Interaction of 14-3-3 with signaling proteins is mediated by the recognition of phosphoserine
17. The structural basis for 14-3-3: Phosphopeptide binding specificity
18. BH3 domain is required for heterodimerization with Bcl-XL and pro-apoptotic activity
19. Autophagy is activated by apoptotic signalling in sympathetic neurons: An alternative mechanism of death execution
20. Nerve growth factor-induced PKB/Akt activity is sustained by phosphoinositide 3-kinase dependent and independent signals in sympathetic neurons