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Translocation of caveolin regulates stretch-induced ERK activity in vascular smooth muscle

https://asahikawa-med.repo.nii.ac.jp/records/3324
https://asahikawa-med.repo.nii.ac.jp/records/3324
0fa22230-c642-49cf-91da-6a8587c288f0
名前 / ファイル ライセンス アクション
211.pdf 211.pdf (431.8 kB)
Item type 学術雑誌論文 / Journal Article_02(1)
公開日 2007-02-14
タイトル
タイトル Translocation of caveolin regulates stretch-induced ERK activity in vascular smooth muscle
言語 en
言語
言語 eng
資源タイプ
資源タイプ journal article
著者 川辺, 淳一

× 川辺, 淳一

ja 川辺, 淳一

ja-Kana カワベ, ジュンイチ

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Okumura, S

× Okumura, S

en Okumura, S

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Lee, MC

× Lee, MC

Lee, MC

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Sadoshima, J

× Sadoshima, J

en Sadoshima, J

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Ishikawa, Y

× Ishikawa, Y

Ishikawa, Y

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著者 ローマ字
Kawabe, Junichi
著者 ローマ字
en
書誌情報 AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY

巻 286, 号 5, p. H1845-H1852, 発行日 2004-05-01
ISSN
収録物識別子タイプ ISSN
収録物識別子 0363-6135
DOI
関連タイプ isIdenticalTo
識別子タイプ DOI
関連識別子 10.1152/ajpheart.00593.2003
リンクURL
内容記述タイプ Other
内容記述 http://ajpheart.physiology.org/cgi/content/abstract/286/5/H1845?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&volume=286&firstpage=H1845&resourcetype=HWCIT | http://ajpheart.physiology.org/cgi/content/abstract/286/5/H1845?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&volume=286&firstpage=H1845&resourcetype=HWCIT
抄録
内容記述タイプ Abstract
内容記述 Mechanical stress contributes to vascular disease related to hypertension. Activation of ERK is key to mediating cellular proliferation and vascular remodeling in response to stretch stress. However, the mechanism by which stretch mediates ERK activation in the vascular tissue is still unclear. Caveolin, a major component of a flasklike invaginated caveolae, acts as an adaptor protein for an integrin-mediated signaling pathway. We found that cyclic stretch transiently induced translocation of caveolin from caveolae to noncaveolar membrane sites in vascular smooth muscle cells (VSMCs). This translocation of caveolin was determined by detergent solubility, sucrose gradient fractionation, and immunocytochemistry. Cyclic stretch induced ERK activation; the activity peaked at 5 min (the early phase), decreased gradually, but persisted up to 120 min (the late phase). Disruption of caveolae by methyl-β-cyclodextrin, decreasing the caveolar caveolin and accumulating the noncaveolar caveolin, enhanced ERK activation in both the early and late phases. When endogenous caveolins were downregulated, however, the late-phase ERK activation was subsided completely. Caveolin, which was translocated to noncaveolar sites in response to stretch, is associated with β_1-integrins as well as with Fyn and Shc, components required for ERK activation. Taken together, caveolin in caveolae may keep ERK inactive, but when caveolin is translocated to noncaveolar sites in response to stretch stress, caveolin mediates stretch-induced ERK activation through an association with β_1-integrins/Fyn/Shc. We suggest that stretch-induced translocation of caveolin to noncaveolar sites plays an important role in mediating stretch-induced ERK activation in VSMCs.
言語 en
注記
内容記述タイプ Other
注記 Kawabe, J; Okumura, S; Lee, MC; Sadoshima, J; Ishikawa, Y, AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 286(5), H1845-H1852, 2004. "Copyright 2004 by the American Physical Society."
\npublisher
言語 en
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内容記述タイプ Other
資源タイプ text
著者版フラグ
出版タイプ VoR
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内容記述タイプ Other
内容記述 application/pdf
ID(XooNIps)
15072971
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1156
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Cite as

川辺, 淳一, Okumura, S, Lee, MC, Sadoshima, J, Ishikawa, Y, n.d., Translocation of caveolin regulates stretch-induced ERK activity in vascular smooth muscle: H1845–H1852 p.

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