{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T20:52:28Z","timestamp":1771015948715,"version":"3.50.1"},"reference-count":91,"publisher":"Rockefeller University Press","issue":"5","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1999,3,8]]},"abstract":"<jats:p>Suppression of gap-junctional communication by various protein kinases, growth factors, and oncogenes frequently correlates with enhanced mitogenesis. The oncogene v-src appears to cause acute closure of gap junction channels. Tyr265 in the COOH-terminal tail of connexin 43 (Cx43) has been implicated as a potential target of v-src, although v-src action has also been associated with changes in serine phosphorylation. We have investigated the mechanism of this acute regulation through mutagenesis of Cx43 expressed in Xenopus laevis oocyte pairs. Truncations of the COOH-terminal domain led to an almost complete loss of response of Cx43 to v-src, but this was restored by coexpression of the independent COOH-terminal polypeptide. This suggests a ball and chain gating mechanism, similar to the mechanism proposed for pH gating of Cx43, and K+ channel inactivation. Surprisingly, we found that v-src mediated gating of Cx43 did not require the tyrosine site, but did seem to depend on the presence of two potential SH3 binding domains and the mitogen-activated protein (MAP) kinase phosphorylation sites within them. Further point mutagenesis and pharmacological studies in normal rat kidney (NRK) cells implicated MAP kinase in the gating response to v-src, while the stable binding of v-src to Cx43 (in part mediated by SH3 domains) did not correlate with its ability to mediate channel closure. This suggests a common link between closure of gap junctions by v-src and other mitogens, such as EGF and lysophosphatidic acid (LPA).<\/jats:p>","DOI":"10.1083\/jcb.144.5.1033","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T16:45:41Z","timestamp":1027701941000},"page":"1033-1045","update-policy":"https:\/\/doi.org\/10.1083\/jcb.crossmarkpolicy","source":"Crossref","is-referenced-by-count":132,"title":["Dissection of the Molecular Basis of pp60v<i>-src<\/i> Induced Gating of Connexin 43 Gap Junction Channels"],"prefix":"10.1083","volume":"144","author":[{"given":"Lan","family":"Zhou","sequence":"first","affiliation":[{"name":"Department of Biological Sciences, State University of New York at Buffalo, Buffalo, New York 14260"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eileen M.","family":"Kasperek","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, State University of New York at Buffalo, Buffalo, New York 14260"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bruce J.","family":"Nicholson","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, State University of New York at Buffalo, Buffalo, New York 14260"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"291","published-online":{"date-parts":[[1999,3,8]]},"reference":[{"key":"2023072900265303500_B1","doi-asserted-by":"crossref","first-page":"573","DOI":"10.1083\/jcb.91.2.573","article-title":"Rapid and reversible reduction of junctional permeability in cells infected with a temperature-sensitive mutant of avian sarcoma virus","volume":"91","author":"Atkinson","year":"1981","journal-title":"J Cell Biol"},{"key":"2023072900265303500_B2","doi-asserted-by":"crossref","first-page":"398","DOI":"10.1126\/science.2447651","article-title":"The cellular srcgene product regulates junctional cell-to-cell communication","volume":"239","author":"Azarnia","year":"1988","journal-title":"Science"},{"key":"2023072900265303500_B3","doi-asserted-by":"crossref","first-page":"8410","DOI":"10.1073\/pnas.88.19.8410","article-title":"Gap junctions formed by connexins 26 and 32 alone and in combination are differently affected by applied voltage [published erratum appears in Proc. 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