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Alliance"],"accepted":{"date-parts":[[2024,5,7]]},"published-print":{"date-parts":[[2024,8]]},"abstract":"<jats:p>\n                    Phosphatidylcholine (PC) is the major membrane phospholipid in most eukaryotic cells. Bi-allelic loss of function variants in\n                    <jats:italic>CHKB<\/jats:italic>\n                    , encoding the first step in the synthesis of PC, is the cause of a rostrocaudal muscular dystrophy in both humans and mice. Loss of sarcolemma integrity is a hallmark of muscular dystrophies; however, how this occurs in the absence of choline kinase function is not known. We determine that in\n                    <jats:italic>Chkb<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice there is a failure of the \u03b17\u03b21 integrin complex that is specific to affected muscle. We observed that in\n                    <jats:italic>Chkb<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    hindlimb muscles there is a decrease in sarcolemma association\/abundance of the PI(4,5)P\n                    <jats:sub>2<\/jats:sub>\n                    binding integrin complex proteins vinculin, and \u03b1-actinin, and a decrease in actin association with the sarcolemma. In cells, pharmacological inhibition of choline kinase activity results in internalization of a fluorescent PI(4,5)P\n                    <jats:sub>2<\/jats:sub>\n                    reporter from discrete plasma membrane clusters at the cell surface membrane to cytosol, this corresponds with a decreased vinculin localization at plasma membrane focal adhesions that was rescued by overexpression of\n                    <jats:italic>CHKB<\/jats:italic>\n                    .\n                  <\/jats:p>","DOI":"10.26508\/lsa.202301956","type":"journal-article","created":{"date-parts":[[2024,5,15]],"date-time":"2024-05-15T11:05:17Z","timestamp":1715771117000},"page":"e202301956","update-policy":"https:\/\/doi.org\/10.26508\/lsa.crossmarkpolicy","source":"Crossref","is-referenced-by-count":3,"title":["Defects in integrin complex formation promote\n                    <i>CHKB<\/i>\n                    -mediated muscular 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