Journal article
Characterisation of mice lacking all functional isoforms of the pro-survival BCL-2 family member A1 reveals minor defects in the haematopoietic compartment
RL Schenk, S Tuzlak, EM Carrington, Y Zhan, S Heinzel, CE Teh, DH Gray, L Tai, AM Lew, A Villunger, A Strasser, MJ Herold
Cell Death and Differentiation | NATURE PUBLISHING GROUP | Published : 2017
DOI: 10.1038/cdd.2016.156
Abstract
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 γδTCR T cells, antigen-experienced conventional as well as regulatory CD4 T cells and conventional dendritic..
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Awarded by Austrian Science Fund
Funding Acknowledgements
We thank all members of the Herold laboratory for their support and advice. G Siciliano, H Johnson and their team for animal husbandry; S Monard and his team for help with flow cytometry unit. This work was supported by a Leukemia Foundation National Research Program PhD Scholarship (to RLS), National Health and Medical Research Council, Australia (program grant 1016701 and fellowship 1020363 to AS) and project grant APP1049720 (to MJH). This work was made possible through Victorian State Government Operational Infrastructure Support and Australian Government National Health and Medical Research Council Independent Research Institutes Infrastructure Support Scheme and by grants from the Austrian Science Fund (FWF), Grant I1298 (FOR-2036) and W1101 (MCBO). ST is supported by a Doc-fellowship from the Austrian Academy of Science (OAW).