Journal
CELL DEATH AND DIFFERENTIATION
Volume 24, Issue 3, Pages 534-545Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2016.156
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Funding
- Leukemia Foundation National Research Program PhD Scholarship
- National Health and Medical Research Council, Australia [1016701, 1020363, APP1049720]
- Austrian Science Fund (FWF) [I1298 (FOR-2036)]
- MCBO [W1101]
- Doc-fellowship from the Austrian Academy of Science (OAW)
- Austrian Science Fund (FWF) [I1298] Funding Source: Austrian Science Fund (FWF)
- Austrian Science Fund (FWF) [I 1298] Funding Source: researchfish
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The pro-survival proteins of the BCL-2 family regulate the survival of all cells, and genetic deletion models for these proteins have revealed which specific BCL-2 family member(s) is/are critical for the survival of particular cell types. A1 is a pro-survival BCL-2-like protein that is expressed predominantly in haematopoietic cells, and here we describe the characterisation of a novel mouse strain that lacks all three functional isoforms of A1 (A1-a, A1-b and A1-d). Surprisingly, complete loss of A1 caused only minor defects, with significant, although relatively small, decreases in gamma delta TCR T cells, antigen-experienced conventional as well as regulatory CD4 T cells and conventional dendritic cells (cDCs). When examining these cell types in tissue culture, only cDC survival was significantly impaired by the loss of A1. Therefore, A1 appears to be a surprisingly redundant pro-survival protein in the haematopoietic system and other tissues, suggesting that its targeting in cancer may be readily tolerated.
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