Journal article
Conditional knockdown of BCL2A1 reveals rate-limiting roles in BCR-dependent B-cell survival
M Sochalska, E Ottina, S Tuzlak, S Herzog, M Herold, A Villunger
Cell Death and Differentiation | NATURE PUBLISHING GROUP | Published : 2016
DOI: 10.1038/cdd.2015.130
Open access
Abstract
Bcl2 family proteins control mitochondrial apoptosis and its members exert critical cell type and differentiation stage-specific functions, acting as barriers against autoimmunity or transformation. Anti-apoptotic Bcl2a1/Bfl1/A1 is frequently deregulated in different types of blood cancers in humans but its physiological role is poorly understood as quadruplication of the Bcl2a1 gene locus in mice hampers conventional gene targeting strategies. Transgenic overexpression of A1, deletion of the A1-a paralogue or constitutive knockdown in the hematopoietic compartment of mice by RNAi suggested rate-limiting roles in lymphocyte development, granulopoiesis and mast cell activation. Here we report..
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Awarded by Australian Academy of Science
Funding Acknowledgements
We are grateful to K Rossi, C Soratroi and I Gaggl for an excellent technical assistance and Bernd Rieder for animal care as well as to V Labi for help with B-cell analysis and discussion. We thank J Zuber and S Lowe for TRE-Ren mice. This work was supported by grants from the Austrian Science Fund (FWF), grant I1298 (FOR-2036) and the MCBO Doctoral College 'Molecular Cell Biology and Oncology' (W1101) and the 'Osterreichische Krebshilfe Tirol'. MH is supported by the National Health and Medical Research Council, Australia project grant APP1049720. ST is supported by a Doc-fellowship from the Austrian Academy of Science (OAW).