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Zfx controls BCR-induced proliferation and survival of B lymphocytes
Measurement Type: 
Transcription Profiling (Microarray)
Design Type: 
Perturbation Design
Genetic Characteristics, Time Point
The development, homeostasis and function of B lymphocytes involve multiple rounds of B cell receptor (BCR)-controlled proliferation and prolonged maintenance. We analyzed the role of transcription factor Zfx, a recently identified regulator of stem cell maintenance, in B cell development and homeostasis. Conditional Zfx deletion in the bone marrow blocked B cell development at the pre-BCR selection checkpoint. Zfx deficiency in peripheral B cells caused impaired generation of the B-1 cell lineage, accelerated B cell turnover, depletion of mature recirculating cells, and delayed T-dependent antibody responses. Zfx-deficient B cells showed normal proximal BCR signaling, but impaired BCR-induced proliferation and survival. This was accompanied by aberrantly enhanced and prolonged integrated stress response, and delayed induction of Cyclin D2 and Bcl-xL proteins. Thus, Zfx restrains the stress response and couples antigen receptor signaling to B cell expansion and maintenance during development and peripheral homeostasis.


Transcription factor Zfx controls BCR-induced proliferation and survival of B lymphocytes.
Arenzana TL, Smith-Raska MR, Reizis B
Blood. 2009 Jun 4; 113(23):5857-67. PMID: 19329779. Abstract
Study metadata (ISA-Tab: