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• W2072393783 abstract "Fas-associated protein with death domain/mediator of receptor induced toxicity (FADD/MORT1) was first described as a transducer of death receptor signalling but was later recognized also to be important for proliferation of T cells. B-cell lymphoma 3 (Bcl-3) is a relatively little understood member of the nuclear factor (NF)-kappaB family of transcription factors. We recently found that Bcl-3 is up-regulated in T cells from mice where FADD function is blocked by a dominant negative transgene (FADD-DN). To understand the importance of this, we generated FADD-DN/bcl-3(-/-) mice. Here, we report that T cells from these mice show massive cell death and severely reduced proliferation in response to T-cell receptor (TCR) stimulation in vitro. Transgenic co-expression of Bcl-2 (FADD-DN/bcl-3(-/-)/vav-bcl-2 mice) rescued the survival but not the proliferation of T cells. FADD-DN/bcl-3(-/-) mice had normal thymocyte numbers but reduced numbers of peripheral T cells despite an increase in cycling T cells in vivo. However, activation of the classical NF-kappaB and extracellular regulated kinase (ERK) pathways and expression of interleukin (IL)-2 mRNA upon stimulation were normal in T cells from FADD-DN/bcl-3(-/-) mice. These data suggest that FADD and Bcl-3 regulate separate pathways that both contribute to survival and proliferation in mouse T cells." @default.
• W2072393783 created "2016-06-24" @default.
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• W2072393783 date "2008-12-01" @default.
• W2072393783 modified "2023-10-14" @default.
• W2072393783 title "FADD and the NF-κB family member Bcl-3 regulate complementary pathways to control T-cell survival and proliferation" @default.
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• W2072393783 doi "https://doi.org/10.1111/j.1365-2567.2008.02869.x" @default.
• W2072393783 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2612552" @default.
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