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• W2124028938 startingPage "603" @default.
• W2124028938 abstract "The pre–T cell receptor (TCR) is expressed early during T cell development and imposes a tight selection for differentiating T cell progenitors. Pre-TCR–expressing cells are selected to survive and differentiate further, whereas pre-TCR− cells are “negatively” selected to die. The mechanisms of pre-TCR–mediated survival are poorly understood. Here, we describe the induction of the antiapoptotic gene BCL2A1 (A1) as a potential mechanism regulating inhibition of pre–T cell death. We characterize in detail the signaling pathway involved in A1 induction and show that A1 expression can induce pre–T cell survival by inhibiting activation of caspase-3. Moreover, we show that in vitro “knockdown” of A1 expression can compromise survival even in the presence of a functional pre-TCR. Finally, we suggest that pre-TCR–induced A1 overexpression can contribute to T cell leukemia in both mice and humans." @default.
• W2124028938 created "2016-06-24" @default.
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• W2124028938 date "2005-02-21" @default.
• W2124028938 modified "2023-09-26" @default.
• W2124028938 title "The BCL2A1 gene as a pre–T cell receptor–induced regulator of thymocyte survival" @default.
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• W2124028938 doi "https://doi.org/10.1084/jem.20041924" @default.
• W2124028938 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2213063" @default.
• W2124028938 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15728238" @default.
• W2124028938 hasPublicationYear "2005" @default.
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