Junctional instability overrides intrinsic quiescence of bul

<!DOCTYPE html> <html lang="ru"> <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="Лучшие ученые" /> <meta name="citation_journal_title" content="Взгляд на стволовые клетки"> <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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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>Отказ от ответственности:</b> Этот реферат был переведен с помощью инструментов искусственного интеллекта и еще не прошел проверку или верификацию</div> <div class="nav social-icons align-items-center"> <p class="m-0">Поделитесь этой статьей:</p> <a class="facebook" title="кликните сюда" target="_blank" href="https://www.facebook.com/sharer.php?u=https://russian.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="кликните сюда" target="_blank" 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