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Junctional instability overrides intrinsic quiescence of bul | 108967

<!DOCTYPE html> <html lang="ja"> <head> <meta charset="utf-8"> <meta name="viewport" content="width=device-width, initial-scale=1"> <title>Junctional instability overrides intrinsic quiescence of bul | 108967</title> <meta name="keywords" content="Avinanda Banerjee, "/> <meta name="description" content="Vinculin, a mechano-transducer associated with both adherens junctions (AJ) and focal adhesions (FA), plays a central role in force transmission through c..108967"/> <meta name="citation_publisher" content="プライムスカラーズ" /> <meta name="citation_journal_title" content="幹細胞に関する洞察"> <meta name="citation_title" content="Junctional instability overrides intrinsic quiescence of bulge stem cells"> <meta name="citation_author" content="Avin" /> <meta name="citation_author" content="a Banerjee" /> <meta name="citation_year" content=""> <meta name="citation_volume" content="7"> <meta name="citation_issue" content="3"> <meta name="citation_abstract" content="Vinculin, a mechano-transducer associated with both adherens junctions (AJ) and focal adhesions (FA), plays a central role in force transmission through cell-cell and cell-substratum contacts. We generated the conditional knockout (KO) of vinculin in murine skin which results in the loss of bulge stem cell (BuSC) quiescence, and promotes continual cycling of the hair follicles. Surprisingly, we find that the AJs in vinculin KO cells are mechanically weak and impaired in force generation despite increased junctional expression of E-cadherin and a-catenin. Mechanistically, we demonstrate that vinculin functions by keeping a-catenin in a stretched/open conformation, which in turn regulates the retention of YAP1, another potent mechano-transducer and regulator of cell proliferation, at the AJs. Altogether, our data provides definitive mechanistic insights into the hitherto unexplored regulatory link between the mechanical stability of cell junctions and contact inhibition-mediated maintenance of BuSC quiescence. 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role="presentation" /> through cell-cell and cell-substratum contacts. We generated the conditional knockout (KO) of vinculin in murine skin which results in the loss<br role="presentation" /> of bulge stem cell (BuSC) quiescence, and promotes continual cycling of the hair follicles. Surprisingly, we find that the AJs in vinculin KO cells<br role="presentation" /> are mechanically weak and impaired in force generation despite increased junctional expression of E-cadherin and a-catenin. Mechanistically,<br role="presentation" /> we demonstrate that vinculin functions by keeping a-catenin in a stretched/open conformation, which in turn regulates the retention of YAP1,<br role="presentation" /> another potent mechano-transducer and regulator of cell proliferation, at the AJs. Altogether, our data provides definitive mechanistic insights<br role="presentation" /> into the hitherto unexplored regulatory link between the mechanical stability of cell junctions and contact inhibition-mediated maintenance of<br role="presentation" /> BuSC quiescence.</p> </p> <div class="alert alert-info text-left"><b>免責事項:</b> この要約は人工知能ツールを使用して翻訳されており、まだレビューまたは確認されていません</div> <div class="nav social-icons align-items-center"> <p class="m-0">この記事をシェアする:</p> <a class="facebook" title="ここをクリック" target="_blank" href="https://www.facebook.com/sharer.php?u=https://japanese.primescholars.com/abstract/junctional-instability-overrides-intrinsic-quiescence-of-bulge-stem-cells-108967.html" rel="noopener"><i class="fab fa-facebook-f"></i></a> <a class="twitter" title="ここをクリック" target="_blank" href="https://twitter.com/share?url=https://japanese.primescholars.com/abstract/junctional-instability-overrides-intrinsic-quiescence-of-bulge-stem-cells-108967.html" rel="noopener"><i class="fab 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