Jabbour, A M; Heraud, J E; Daunt, C P; Kaufmann, T; Sandow, J; O'Reilly, L A; Callus, B A; Lopez, A; Strasser, A; Vaux, D L; Ekert, P G (2009). Puma indirectly activates Bax to cause apoptosis in the absence of Bid or Bim. Cell death and differentiation, 16(4), pp. 555-63. Basingstoke: Nature Publishing Group 10.1038/cdd.2008.179
Full text not available from this repository.Bcl-2 family members regulate apoptosis in response to cytokine withdrawal and a broad range of cytotoxic stimuli. Pro-apoptotic Bcl-2 family members Bax and Bak are essential for apoptosis triggered by interleukin-3 (IL-3) withdrawal in myeloid cells. The BH3-only protein Puma is critical for initiation of IL-3 withdrawal-induced apoptosis, because IL-3-deprived Puma(-/-) cells show increased capacity to form colonies when IL-3 is restored. To investigate the mechanisms of Puma-induced apoptosis and the interactions between Puma and other Bcl-2 family members, we expressed Puma under an inducible promoter in cells lacking one or more Bcl-2 family members. Puma rapidly induced apoptosis in cells lacking the BH3-only proteins, Bid and Bim. Puma expression resulted in activation of Bax, but Puma killing was not dependent on Bax or Bak alone as Puma readily induced apoptosis in cells lacking either of these proteins, but could not kill cells deficient for both. Puma co-immunoprecipitated with the anti-apoptotic Bcl-2 family members Bcl-x(L) and Mcl-1 but not with Bax or Bak. These data indicate that Puma functions, in the context of induced overexpression or IL-3 deprivation, primarily by binding and inactivating anti-apoptotic Bcl-2 family members.
Item Type: |
Journal Article (Original Article) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Pharmacology |
UniBE Contributor: |
Kaufmann, Thomas (B) |
ISSN: |
1350-9047 |
Publisher: |
Nature Publishing Group |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 15:10 |
Last Modified: |
29 Mar 2023 23:33 |
Publisher DOI: |
10.1038/cdd.2008.179 |
PubMed ID: |
19079139 |
Web of Science ID: |
000264176000005 |
URI: |
https://boris.unibe.ch/id/eprint/30683 (FactScience: 194948) |
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