| First Author | Schenk RL | Year | 2017 |
| Journal | Cell Death Differ | Volume | 24 |
| Issue | 3 | Pages | 534-545 |
| PubMed ID | 28085150 | Mgi Jnum | J:258915 |
| Mgi Id | MGI:6140866 | Doi | 10.1038/cdd.2016.156 |
| Citation | Schenk RL, et al. (2017) Characterisation of mice lacking all functional isoforms of the pro-survival BCL-2 family member A1 reveals minor defects in the haematopoietic compartment. Cell Death Differ 24(3):534-545 |
| abstractText | 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 gammadeltaTCR 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. |
