卵泡闭锁
MAPK/ERK通路
细胞生物学
激酶
生物
p38丝裂原活化蛋白激酶
蛋白激酶A
细胞凋亡
信号转导
颗粒细胞
癌症研究
卵泡期
卵泡
内分泌学
遗传学
作者
AT Peter,N. Dhanasekaran
标识
DOI:10.1046/j.1439-0531.2003.00438.x
摘要
Recent studies suggest that ovarian follicular atresia is associated with DNA fragmentation and degeneration of granulosa cells, the hallmark of programmed cell death or apoptosis. Apoptosis of granulosa cells play a major role in follicular atresia. These studies have also demonstrated the involvement of tumour suppressors, apoptotic proteins and survival factors. These factors contribute to the developmental decision as to whether the ovarian follicles mature or undergo atresia. However, the precise temporal and molecular events involved in the apoptotic pathways in this process need to be elucidated. The present report summarizes the role of Jun N-terminal kinase (JNK), p38 mitogen activated protein kinase (p38 MAPK), and extracellular-signal regulated kinase (ERK)-signalling module in the regulation of pro- and anti-apoptotic factors of the granulosa cells in regulating follicular atresia. The findings presented here suggest that the loss of tropic hormone support is translated into the attenuation of Raf-1-MAPK/ERK kinase (MEK)-ERK-signalling pathway of the granulosa cells and this results in the decreased phosphorylation of the pro-apoptotic BAD.
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