Bcl-XL affects Ca2+ homeostasis by altering expression of inositol 1,4,5-trisphosphate receptors.

Li C; Fox CJ; Master SRBindokas VPChodosh LAThompson CB

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Bcl-XL affects Ca2+ homeostasis by altering expression of inositol 1,4,5-trisphosphate receptors.

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An oligonucleotide-based microarray analysis of 9,500 genes and expressed sequence tags (ESTs) demonstrated that the type 1 inositol 1,4,5-trisphosphate receptor (IP(3)R) was significantly down-regulated in Bcl-X(L)-expressing as compared with control cells. This result was confirmed at the mRNA and protein levels by Northern and Western blot analyses of two independent hematopoietic cell lines and murine primary T cells. Bcl-X(L) expression resulted in a dose-dependent decrease in IP(3)R protein. IP(3)R expression is regulated as part of a mitochondrion-to-nucleus stress-responsive pathway. The uncoupling of mitochondrial oxidative phosphorylation resulted in induction of binding of the transcription factor NFATc2 to the IP(3)R promoter and transcriptional activation of IP(3)R. Expression of Bcl-X(L) led to a decreased induction of both NFATc2 DNA binding to the IP(3)R promoter and IP(3)R expression in response to the inhibition of mitochondrial oxidative phosphorylation. The Bcl-X(L)-dependent decrease in IP(3)R expression also correlated with a reduced T cell antigen receptor ligation-induced Ca(2+) flux in Bcl-X(L) transgenic murine T cells, and microsomal vesicles prepared from Bcl-X(L)-overexpressing cells exhibited lower IP(3)-mediated Ca(2+) release capacity. Furthermore, reintroducing IP(3)R into Bcl-X(L)-transfected cells partially reversed Bcl-X(L)-dependent anti-apoptotic activity. These results suggest that even under non-apoptotic conditions, expression of Bcl-2-family proteins influences a signaling network that links changes in mitochondrial metabolism to alterations in nuclear gene expression.

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《Proceedings of the National Academy of Sciences of the United States of America》 |2002年第15期|9830-9835|共6页
作者
Li C; Fox CJ; Master SRBindokas VPChodosh LAThompson CB;
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作者单位

Abramson Family Cancer Research Institute, Department of Cancer Biology, and Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104;

and Department of Neurobiology, Pharmacology and Physiology, University of Chicago, Chicago, IL 6;

cbi.upenn.edu;

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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种英语
中图分类自然科学总论;
关键词
L; T-Lymphocytes; T淋巴细胞;

Bcl-XL affects Ca2+ homeostasis by altering expression of inositol 1,4,5-trisphosphate receptors.

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