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	β-actin is required for mitochondria clustering and ROS generation in TNF-induced, caspase-independent cell death
	Li, JQ ; Li, QX ; Li QX(李勤喜) ; Xie, CC ; Zhou, HM ; Zhou HM(周化民) ; Wang, YQ ; Wang YQ(王义权) ; Zhang, N ; Shao, HJ ; Chan, SC（Department of Biochemistry, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong） ; Peng, XX ; Peng XX(彭宣宪) ; Lin, SC ; Lin SC(林圣彩) ; Han, JH ; Han JH(韩家淮)
	2004
关键词	TNF beta-actin necrosis ROS
英文摘要	Tumor necrosis factor (TNF)-alpha induces caspase-independent cell death in the fibrosarcoma cell line L929. This cell death has a necrotic phenotype and is dependent on production of reactive oxygen species (ROS) in the mitochondria. To identify genes involved in this TNF-induced, ROS-dependent cell death pathway, we utilized retrovirus insertion-mediated random mutagenesis to generate TNF-resistant L929 cell lines and we subsequently identified genes whose mutations are responsible for the TNF-resistant phenotype. In one such resistant line, beta-actin was disrupted by viral insertion, and subsequent reconstitution of P-actin expression levels in the mutant line Actin(mut) restored its sensitivity to TNF Resistance to TNF in Actin(mut) cells is signal specific since the sensitivity to other death stimuli is either unchanged or even increased. Comparable NF-kappaB activation and p38 phosphorylation in TNF-treated wild-type and Actin(mut) cells also indicates that reduced expression of actin only selectively blocked some of the TNF-induced cellular changes. Actin cleavage involved in apoptosis does not occur in TNF-treated L929 cell death, as in HeLa cells. Consistent over-expression of a caspase-cleaved product, a 15 kDa actin fragment, had no effect on TNF-induced necrosis of L929 cell. By contrast, TNF-induced mitochondria clustering and ROS production were dramatically reduced in Actinmut cells, indicating that actin-deficiency-mediated TNF resistance is most likely due to impaired mitochondrial responses to TNF stimulation. Our findings suggest that a full complement of actin is required for transduction of a cell death signal to mitochondria in TNF-treated L929 cells.
语种	英语
出版者	COMPANY OF BIOLOGISTS LTD
内容类型	期刊论文
源URL	[http://dx.doi.org/doi:10.1242/ jcs.01339]
专题	生命科学－已发表论文
推荐引用方式 GB/T 7714	Li, JQ,Li, QX,Li QX,et al. β-actin is required for mitochondria clustering and ROS generation in TNF-induced, caspase-independent cell death[J],2004.
APA	Li, JQ.,Li, QX.,李勤喜.,Xie, CC.,Zhou, HM.,...&韩家淮.(2004).β-actin is required for mitochondria clustering and ROS generation in TNF-induced, caspase-independent cell death..
MLA	Li, JQ,et al."β-actin is required for mitochondria clustering and ROS generation in TNF-induced, caspase-independent cell death".(2004).

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