期刊
BIOCHEMICAL JOURNAL
卷 399, 期 -, 页码 335-342出版社
PORTLAND PRESS LTD
DOI: 10.1042/BJ20060612
关键词
apoptosis; cell cycle; cellular inhibitor of apoptosis protein (cIAP); inhibitor of apoptosis protein (IAP); mitosis; nuclear factor KB (NF-kappa B)
cIAP2 (cellular inhibitor of apoptosis protein 2) is induced by NF-kappa B (nuclear factor kappa B) when cells need to respond quickly to different apoptotic stimuli. A recent study using cDNA microarray technology has suggested that cIAP2 transcription is regulated in a cell cycle-dependent manner, although the mechanism for such regulation is unknown. In this study, we confirmed the cell cycle-dependent regulation of cIAP2 expression at both the mRNA and protein levels. Additionally, we found that a bipartite CDE (cell cycle-dependent element)/CHR (cell cycle gene homology region) element in the cIAP2 promoter mediates cIAP2 gene activation in G2/M phase. Cell cycle-dependent G2/M-phase-specific cIAP2 expression is enhanced by NF-kappa B activation, and selective down-regulation of cIAP2 causes cells blocked in mitosis with nocodazole to become susceptible to apoptosis, indicating that the G2/M-phase-specific expression of cIAP2 contributes to the survival of mitotically arrested cells. Our studies describing the NF-kappa B-independent G2/M-phase-specific expression of cIAP2 will help in further understanding the molecular basis of cIAP2 overexpression in a variety of human cancers.
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