1999年8月
Activation of Rac1 increases c-Jun NH2-terminal kinase activity and DNA fragmentation in a calcium-dependent manner in rat myoblast cell line H9c2
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- ,
- ,
- 巻
- 262
- 号
- 2
- 開始ページ
- 350
- 終了ページ
- 354
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1006/bbrc.1999.1218
- 出版者・発行元
- ACADEMIC PRESS INC
We examined the role of intracellular Ca2+ in c-Jun NH2-terminal kinase (JNK) activation and DNA fragmentation in the rat myoblast cell line H9c2 using small GTP-binding protein Rad. A constitutively active mutant of Rad (V12-Rac1) increased JNK-responsive gene expression 6-fold, although this increase was attenuated by the intracellular Ca2+ chelator BAPTA-AM. V12-Rac1 also increased the number of DNA fragmentated cells. However, V12-Rac1-mediated JNK activation was not affected by BAPTA-AM as determined by direct measurement of active forms, and V12-Rac1 did not affect intracellular Ca2+ concentration. These results suggest that Rad can activate JNK and induces cell injury, but [Ca2+](i) is necessary for V12-Rac1 to induce DNA fragmentation downstream Of JNK activation. (C) 1999 Academic Press.
- リンク情報
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- DOI
- https://doi.org/10.1006/bbrc.1999.1218
- CiNii Articles
- http://ci.nii.ac.jp/naid/30017786263
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/10462478
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000082343000008&DestApp=WOS_CPL
- ID情報
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- DOI : 10.1006/bbrc.1999.1218
- ISSN : 0006-291X
- CiNii Articles ID : 30017786263
- PubMed ID : 10462478
- Web of Science ID : WOS:000082343000008