{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T09:11:04Z","timestamp":1790759464607,"version":"4.1.0"},"reference-count":35,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2016,4,18]],"date-time":"2016-04-18T00:00:00Z","timestamp":1460937600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"JSPS KAKENHI","award":["25460357"],"award-info":[{"award-number":["25460357"]}]},{"name":"Grants-in-Aid of the Translational Research Network Program","award":["B-15"],"award-info":[{"award-number":["B-15"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes to Cells"],"published-print":{"date-parts":[[2016,6]]},"abstract":"<jats:p>The neuromuscular junction (NMJ) is a synapse between a motor neuron and skeletal muscle and is required for muscle contraction. The formation and maintenance of NMJs are governed by the muscle\u2010specific receptor tyrosine kinase MuSK. We previously showed that the muscle cytoplasmic protein Dok\u20107 is an essential activator of MuSK. Indeed, mice lacking either Dok\u20107 or MuSK form no NMJs, and defects in the human <jats:italic>DOK7<\/jats:italic> gene underlie a congenital myasthenic syndrome (an NMJ disorder). However, it remains unproven whether Dok\u20107 is required for the postnatal maintenance of NMJs. In this study, we generated recombinant adeno\u2010associated virus (AAV) vectors encoding short hairpin RNAs targeting the mouse <jats:italic>dok\u20107<\/jats:italic> gene (AAV\u2010shD7). Systemic administration of AAV\u2010shD7 into 2\u2010week\u2010old mice down\u2010regulated <jats:italic>dok\u20107<\/jats:italic> expression in muscle and induced myasthenic symptoms including reduction in body weight and motor function. Moreover, AAV\u2010shD7 treatment suppressed MuSK\u2010dependent gene expression of NMJ components and reduced the size of NMJs. These results demonstrate that correct, physiological levels of <jats:italic>dok\u20107<\/jats:italic> expression are required for the postnatal maintenance of NMJs.<\/jats:p>","DOI":"10.1111\/gtc.12370","type":"journal-article","created":{"date-parts":[[2016,4,19]],"date-time":"2016-04-19T03:17:52Z","timestamp":1461035872000},"page":"670-676","source":"Crossref","is-referenced-by-count":34,"title":["Postnatal knockdown of <i>dok\u20107<\/i> gene expression in mice causes structural defects in neuromuscular synapses and myasthenic pathology"],"prefix":"10.1111","volume":"21","author":[{"given":"Takahiro","family":"Eguchi","sequence":"first","affiliation":[{"name":"Division of Genetics Department of Cancer Biology The Institute of Medical Science The University of Tokyo Tokyo 108\u20108639 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tohru","family":"Tezuka","sequence":"additional","affiliation":[{"name":"Division of Genetics Department of Cancer Biology The Institute of Medical Science The University of Tokyo Tokyo 108\u20108639 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sadanori","family":"Miyoshi","sequence":"additional","affiliation":[{"name":"Division of Genetics Department of Cancer Biology The Institute of Medical Science The University of Tokyo Tokyo 108\u20108639 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuji","family":"Yamanashi","sequence":"additional","affiliation":[{"name":"Division of Genetics Department of Cancer Biology The Institute of Medical Science The University of Tokyo Tokyo 108\u20108639 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2016,4,18]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.4610-11.2012"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.1250744"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.1733-14.2014"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.1130837"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.gt.3303029"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddn251"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/dds198"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrn3821"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(14)70201-7"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2007.02.035"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/dds483"},{"key":"e_1_2_6_13_1","doi-asserted-by":"publisher","DOI":"10.1038\/85899"},{"key":"e_1_2_6_14_1","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1977710"},{"key":"e_1_2_6_15_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M708607200"},{"key":"e_1_2_6_16_1","first-page":"1437","article-title":"Targeted mutation of mouse skeletal muscle sodium channel produces myotonia and potassium\u2010sensitive weakness","volume":"118","author":"Hayward L.J.","year":"2008","journal-title":"J. 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