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- W2272541102 abstract "Abstract T cells depend on the careful regulation of apoptosis for normal development, homeostasis and immune response. The Bcl-2 family of proteins has been shown to play critical roles regulating T cell apoptotic pathways. The anti-apoptotic proteins Bcl-2 and Mcl-1 each display a unique expression pattern throughout the lifespan of a T cell and both have been shown to be essential for T cell survival at multiple stages. However, it is unclear whether these proteins function in the same or separate molecular pathways. Here, we use genetic models to show that Mcl-1, through antagonism of Bak, has a unique function from Bcl-2 at multiple stages of thymocyte development. Loss of Bak rescues the death of Mcl-1-deficient thymocytes at the double negative and single positive stages. Loss of Bax, however, does not rescue Mcl-1-deficient thymocytes. Neither over-expression of Bcl-2 nor loss of the BH3-only protein Bim rescues the death of Mcl-1-deficient thymocytes. Interestingly, loss of Bak does not rescue activated T cells in an in vitro Mcl-1 deletion system, thus mechanisms may differ at different stages. These data indicate non-overlapping and distinct roles for Mcl-1 and Bcl-2 in T cells. This work was supported by grants from the NIH." @default.
- W2272541102 created "2016-06-24" @default.
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- W2272541102 date "2009-04-01" @default.
- W2272541102 modified "2023-09-26" @default.
- W2272541102 title "Mcl-1 promotes T cell survival independently of Bcl-2 through interaction with Bak (84.19)" @default.
- W2272541102 doi "https://doi.org/10.4049/jimmunol.182.supp.84.19" @default.
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