{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T07:28:20Z","timestamp":1772090900795,"version":"3.50.1"},"reference-count":22,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2013,11,20]],"date-time":"2013-11-20T00:00:00Z","timestamp":1384905600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes to Cells"],"published-print":{"date-parts":[[2014,1]]},"abstract":"<jats:p>After peripheral nerve injury, Schwann cells gain a migratory phenotype and remodel their extracellular matrix to provide a supportive environment for axonal regeneration. The soluble neuregulin\u20101 isoform, that is, glial growth factor (<jats:styled-content style=\"fixed-case\">GGF<\/jats:styled-content>), is expressed in regenerating axons of injured peripheral nerves and regulates Schwann cell motility by activating the ErbB family of tyrosine kinase receptors, but how <jats:styled-content style=\"fixed-case\">GGF<\/jats:styled-content>\/ErbB signaling contributes to Schwann cell motility remains unclear. Here, we show that <jats:styled-content style=\"fixed-case\">GGF<\/jats:styled-content> stimulates Schwann cell migration by inducing the formation of a protein complex containing the fibronectin receptor \u03b15\u03b21 integrin, ErbB2, and focal adhesion kinase (<jats:styled-content style=\"fixed-case\">FAK<\/jats:styled-content>). ErbB2 co\u2010localizes and co\u2010immunoprecipitates with the focal complex members including \u03b15\u03b21 integrin and <jats:styled-content style=\"fixed-case\">FAK<\/jats:styled-content> after <jats:styled-content style=\"fixed-case\">GGF<\/jats:styled-content> treatment. These effects of <jats:styled-content style=\"fixed-case\">GGF<\/jats:styled-content> appear to involve <jats:styled-content style=\"fixed-case\">FAK<\/jats:styled-content> activation, which occurs downstream of ErbB2 stimulation. <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>i\u2010mediated down\u2010regulation of \u03b15 integrin expression in primary cultured Schwann cells resulted in significantly decreased interaction between <jats:styled-content style=\"fixed-case\">FAK<\/jats:styled-content> and ErbB2, as well as decreased <jats:styled-content style=\"fixed-case\">GGF<\/jats:styled-content>\u2010induced migration. An increase in the \u03b15\u03b21 integrin\u2013ErbB2\u2013<jats:styled-content style=\"fixed-case\">FAK<\/jats:styled-content> complex formation was observed in injured nerve Schwann cells, but not uninjured control. Taken together, these data suggest that <jats:styled-content style=\"fixed-case\">GGF<\/jats:styled-content> plays an important modulatory role in Schwann cell migration after nerve crush by inducing \u03b15\u03b21 integrin\u2013ErbB2\u2013<jats:styled-content style=\"fixed-case\">FAK<\/jats:styled-content> complex formation.<\/jats:p>","DOI":"10.1111\/gtc.12108","type":"journal-article","created":{"date-parts":[[2013,11,21]],"date-time":"2013-11-21T02:16:59Z","timestamp":1385000219000},"page":"66-77","source":"Crossref","is-referenced-by-count":24,"title":["Neuregulin\u20101\/glial growth factor stimulates <scp>S<\/scp>chwann cell migration by inducing \u03b15 \u03b21 integrin\u2013ErbB2\u2013focal adhesion kinase complex formation"],"prefix":"10.1111","volume":"19","author":[{"given":"Shuji","family":"Wakatsuki","sequence":"first","affiliation":[{"name":"Department of Peripheral Nervous System Research National Institute of Neuroscience National Center of Neurology and Psychiatry 4\u20101\u20101 Ogawa\u2010higashi Kodaira Tokyo 187\u20108502 Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Toshiyuki","family":"Araki","sequence":"additional","affiliation":[{"name":"Department of Peripheral Nervous System Research National Institute of Neuroscience National Center of Neurology and Psychiatry 4\u20101\u20101 Ogawa\u2010higashi Kodaira Tokyo 187\u20108502 Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Atsuko","family":"Sehara\u2010Fujisawa","sequence":"additional","affiliation":[{"name":"Department of Growth Regulation Institute for Frontier Medical Sciences Kyoto University Kawahara\u2010cho 53, Shogo\u2010in, Sakyo\u2010ku Kyoto 606\u20108507 Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2013,11,20]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(02)00617-7"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.yexcr.2008.10.035"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1002\/glia.20753"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0053444"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.20-10-03776.2000"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1006\/dbio.2001.0213"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1080\/15216540211470"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)00971-6"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1002\/glia.20761"},{"key":"e_1_2_6_11_1","doi-asserted-by":"crossref","first-page":"767","DOI":"10.1242\/dev.116.3.767","article-title":"Regulation 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