NOTCH2 stimulates transcription of FCER2 (CD23A)

Transient transfection of a human pre-B-cell line REH with a vector encoding recombinant rat NICD2 induces endogenous FCER2 transcription. Overexpression of FCER2 (CD23A) is a hallmark of B-cell chronic lymphocytic leukemia (B-CLL) and correlates with the malfunction of apoptosis, which is thought be an underlying mechanism of B-CLL development. The Epstein-Barr virus protein EBNA2 can also activate FCER2 transcription through RBPJ promoter elements, possibly by mimicking NOTCH2 signaling (Hubmann et al. 2002).

瞬时转染人前B细胞系REH以编码重组大鼠NICD2的载体，可诱导内源性FCER2（CD23A）转录。FCER2（CD23A）的过表达是B细胞慢性淋巴细胞白血病（B-CLL）的特征性标志，并与细胞凋亡功能障碍相关，而细胞凋亡功能障碍被认为是B-CLL发展的潜在机制。爱泼斯坦-巴尔病毒蛋白EBNA2亦可通过RBPJ启动子元件激活FCER2转录，可能通过模拟NOTCH2信号（Hubmann等，2002年）的方式实现。