{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T17:20:29Z","timestamp":1792084829055,"version":"4.4.0"},"reference-count":52,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2012,9,28]],"date-time":"2012-09-28T00:00:00Z","timestamp":1348790400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000027","name":"National Institute on Alcohol Abuse and Alcoholism","doi-asserted-by":"crossref","award":["2R01AA012974"],"award-info":[{"award-number":["2R01AA012974"]}],"id":[{"id":"10.13039\/100000027","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Medical Research Service, Department of Veterans Affairs"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2012,11]]},"abstract":"Abstract<\/jats:title>\n \n Pre\u2010natal alcohol exposure causes fetal alcohol spectrum disorders (\n FASD<\/jats:styled-content>\n ), the most common, preventable cause of developmental disability. The developing cerebellum is particularly vulnerable to the effects of ethanol. We reported that ethanol inhibits the stimulation of axon outgrowth in cerebellar granule neurons (\n CGN<\/jats:styled-content>\n ) by\n NAP<\/jats:styled-content>\n , an active motif of activity\u2010dependent neuroprotective protein (\n ADNP<\/jats:styled-content>\n ), by blocking\n NAP<\/jats:styled-content>\n activation of Fyn kinase and its downstream signaling molecule, the scaffolding protein Cas. Here, we asked whether ethanol inhibits the stimulation of axon outgrowth by diverse axon guidance molecules through a common action on the Src family kinases (\n SFK<\/jats:styled-content>\n ). We first demonstrated that netrin\u20101, glial cell line\u2010derived neurotrophic factor (\n GDNF<\/jats:styled-content>\n ), and neural cell adhesion molecule L1 stimulate axon outgrowth in\n CGN<\/jats:styled-content>\n s by activating\n SFK<\/jats:styled-content>\n , Cas, and extracellular signal\u2010regulated kinase 1 and 2 (\n ERK<\/jats:styled-content>\n 1\/2). The specific\n SFK<\/jats:styled-content>\n inhibitor,\n PP<\/jats:styled-content>\n 2, blocked the stimulation of axon outgrowth and the activation of the\n SFK<\/jats:styled-content>\n \u2010Cas\u2010\n ERK<\/jats:styled-content>\n 1\/2 signaling pathway by each of these axon\u2010guidance molecules. In contrast, brain\u2010derived neurotrophic factor (\n BDNF<\/jats:styled-content>\n ) stimulated axon outgrowth and activated\n ERK<\/jats:styled-content>\n 1\/2 without first activating\n SFK<\/jats:styled-content>\n or Cas. Clinically relevant concentrations of ethanol inhibited axon outgrowth and the activation of the\n SFK<\/jats:styled-content>\n \u2010Cas\u2010\n ERK<\/jats:styled-content>\n 1\/2 pathway by netrin\u20101,\n GDNF<\/jats:styled-content>\n , and L1, but did not disrupt\n BDNF<\/jats:styled-content>\n \u2010induced axon outgrowth or\n ERK<\/jats:styled-content>\n 1\/2 activation. These results indicate that\n SFK<\/jats:styled-content>\n , but not\n ERK<\/jats:styled-content>\n 1\/2, is a primary target for ethanol inhibition of axon outgrowth. The ability of ethanol to block the convergent activation of the\n SFK<\/jats:styled-content>\n \u2010Cas\u2010\n ERK<\/jats:styled-content>\n 1\/2 pathway by netrin\u20101,\n GDNF<\/jats:styled-content>\n , L1, and\n ADNP<\/jats:styled-content>\n could contribute significantly to the pathogenesis of\n FASD<\/jats:styled-content>\n .\n <\/jats:p>","DOI":"10.1111\/j.1471-4159.2012.07954.x","type":"journal-article","created":{"date-parts":[[2012,8,28]],"date-time":"2012-08-28T04:17:11Z","timestamp":1346127431000},"page":"602-612","source":"Crossref","is-referenced-by-count":23,"title":["Retracted:<\/i>\n Ethanol disrupts axon outgrowth stimulated by netrin\u20101,\n GDNF<\/scp>\n , and L1 by blocking their convergent activation of Src family kinase signaling"],"prefix":"10.1111","volume":"123","author":[{"given":"Suzhen","family":"Chen","sequence":"first","affiliation":[{"name":"VA Boston Healthcare System and Department of Neurology Harvard Medical School West Roxbury MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael E.","family":"Charness","sequence":"additional","affiliation":[{"name":"VA Boston Healthcare System and Department of Neurology Harvard Medical School West Roxbury MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2012,9,28]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrn812"},{"key":"e_1_2_6_3_1","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.274.19.13264"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0169-328X(99)00217-X"},{"key":"e_1_2_6_5_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0807758105"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1097-4695(19990215)38:3<428::AID-NEU10>3.0.CO;2-6"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1044-7431(02)00014-3"},{"key":"e_1_2_6_8_1","doi-asserted-by":"publisher","DOI":"10.1159\/000084528"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng1197-346"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.tcb.2006.03.003"},{"key":"e_1_2_6_11_1","first-page":"300","article-title":"Calculation of blood alcohol concentration (BAC) by sex, weight, number of drinks and time","volume":"78","author":"Fisher H. 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