Journal article

The Zinc-finger protein ASCIZ regulates B cell development via DYNLL1 and Bim

Sabine Jurado, Kimberly Gleeson, Kristy O'Donnell, David J Izon, Carl R Walkley, Andreas Strasser, David M Tarlinton, Joerg Heierhorst



Developing B lymphocytes expressing defective or autoreactive pre-B or B cell receptors (BCRs) are eliminated by programmed cell death, but how the balance between death and survival signals is regulated to prevent immunodeficiency and autoimmunity remains incompletely understood. In this study, we show that absence of the essential ATM (ataxia telangiectasia mutated) substrate Chk2-interacting Zn(2+)-finger protein (ASCIZ; also known as ATMIN/ZNF822), a protein with dual functions in the DNA damage response and as a transcription factor, leads to progressive cell loss from the pre-B stage onwards and severely diminished splenic B cell numbers in mice. This lymphopenia cannot be suppressed b..

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Funding Acknowledgements

This work was supported by grants and fellowships from the National Health and Medical Research Council of Australia (NHMRC) to J. Heierhorst, D.J. Izon, C. R. Walkley, D. M. Tarlinton, and A. Strasser, a Melbourne University International Fee Remission Scholarship and a partial PhD scholarship from the Cooperative Research Centre Cancer Therapeutics to S. Jurado, and in part by the Victorian Government's Operational Infrastructure Support Program and Australian Government NHMRC IRIIS. C. R. Walkley is the Phillip Desbrow Senior Research Fellow of the Leukemia Foundation.