期刊
IMMUNITY
卷 26, 期 4, 页码 421-431出版社
CELL PRESS
DOI: 10.1016/j.immuni.2007.03.010
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资金
- Intramural NIH HHS Funding Source: Medline
GA binding protein (GABP) is a ubiquitously expressed Ets-family transcription factor that critically regulates the expression of the interleukin-7 receptor alpha chain (IL-7R alpha) in T cells, whereas it is dispensable for IL-7R alpha expression in fetal liver B cells. Here we showed that deficiency of GABP alpha, the DNA-binding subunit of GABP, resulted in profoundly defective B cell development and a compromised humoral immune response, in addition to thymic developmental defects. Furthermore, the expression of Pax5 and Pax5 target genes such as Cd79a was greatly diminished in GABP alpha-deficient B cell progenitors, pro-B, and mature B cells. GABP could bind to the regulatory regions of Pax5 and Cd79a in vivo. Thus, GABP is a key regulator of B cell development, maturation, and function.
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