How adhesion signals reach a mitochondrial conclusion - ECM regulation of apoptosis

How adhesion signals reach a mitochondrial conclusion - ECM regulation of apoptosis
复制标题

DOI:
10.1016/j.ceb.2009.05.009
复制
发表时间:
2009-10-01
影响因子:
7.5
通讯作者:
Lindsay, Jennefer
Lindsay, Jennefer
中科院分区:
生物学2区
文献类型:
--
作者:
Gilmore, Andrew P.;Owens, Thomas W.;Lindsay, Jennefer

文献摘要

被引文献

相似文献

后生动物的一个基本方面是细胞识别其在组织内的位置背景的能力。这对于发育和稳态都很重要,其中细胞增殖、分化和凋亡受到严格控制以形成和维持组织。关于细胞如何接收和解释粘附介导的信号已经产生了很多信息。非受体酪氨酸激酶 Fak(粘着斑激酶)在粘附介导的信号传导(包括其在生存中的作用)方面受到了广泛关注。抑制细胞凋亡的默认途径需要生存信号。细胞凋亡信号传导的最终结果是将因子从线粒体释放到细胞质中。控制细胞凋亡的明确信号通路如何汇聚到线粒体上是一个有许多未解决问题的领域。
A fundamental aspect in metazoans is the ability of a cell to recognise its positional context within a tissue. This is important in both development and homeostasis, where cell proliferation, differentiation and apoptosis are strictly controlled to form and maintain tissues. Much information has been generated on how cells receive and interpret adhesion-mediated signals. The non-receptor tyrosine kinase, Fak (focal adhesion kinase) has received much attention with regard to adhesion mediated signalling, including its role in survival. Survival signals are required to suppress the default pathway of apoptosis. The ultimate outcome of apoptotic signalling is the release of factors from the mitochondria into the cytosol. How the defined signalling pathways that control apoptosis converge on the mitochondria is an area with many unresolved questions.