Rabih S Talhouk, Antoine A Khalil, Rachid Bajjani, Gilbert J Rahme, Marwan E El-Sabban
{"title":"间隙连接介导CID-9乳腺上皮细胞中stat5非依赖性β-酪蛋白的表达。","authors":"Rabih S Talhouk, Antoine A Khalil, Rachid Bajjani, Gilbert J Rahme, Marwan E El-Sabban","doi":"10.3109/15419061.2011.639468","DOIUrl":null,"url":null,"abstract":"<p><p>Crosstalk between gap junction intracellular communication (GJIC), STAT5 and OCT-1 in gap junction (GJ)-dependent β-casein expression was investigated. CID-9 mammary cells plated with prolactin on non-adherent substratum (poly-HEMA) expressed β-casein independent of STAT5 only in the presence of the GJIC inducer, cAMP. Nuclear STAT5 levels were not detectable. By contrast, cells on EHS-drip expressed β-casein in a STAT5-dependent manner and nuclear STAT5 levels were up-regulated. A 75 kDa OCT-1 isoform was detected in conditions that induced β-casein expression regardless of substratum. Interestingly, 40 and 28 kDa OCT-1 isoforms were induced in cells on polyHEMA with cAMP. Electrophoretic mobility shift assays (EMSA) for OCT-1 revealed two band shifts in cells on polyHEMA with cAMP and on EHS-drip, which were repressed by the GJIC inhibitor, 18α-GA. These studies demonstrated that mammary cells on polyHEMA expressed β-casein in response to prolactin in a pathway that involves GJIC and OCT-1 and is independent of STAT5 nuclear translocation.</p>","PeriodicalId":55269,"journal":{"name":"Cell Communication and Adhesion","volume":"18 5","pages":"104-16"},"PeriodicalIF":0.0000,"publicationDate":"2011-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/15419061.2011.639468","citationCount":"3","resultStr":"{\"title\":\"Gap junctions mediate STAT5-independent β-casein expression in CID-9 mammary epithelial cells.\",\"authors\":\"Rabih S Talhouk, Antoine A Khalil, Rachid Bajjani, Gilbert J Rahme, Marwan E El-Sabban\",\"doi\":\"10.3109/15419061.2011.639468\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Crosstalk between gap junction intracellular communication (GJIC), STAT5 and OCT-1 in gap junction (GJ)-dependent β-casein expression was investigated. CID-9 mammary cells plated with prolactin on non-adherent substratum (poly-HEMA) expressed β-casein independent of STAT5 only in the presence of the GJIC inducer, cAMP. Nuclear STAT5 levels were not detectable. By contrast, cells on EHS-drip expressed β-casein in a STAT5-dependent manner and nuclear STAT5 levels were up-regulated. A 75 kDa OCT-1 isoform was detected in conditions that induced β-casein expression regardless of substratum. Interestingly, 40 and 28 kDa OCT-1 isoforms were induced in cells on polyHEMA with cAMP. Electrophoretic mobility shift assays (EMSA) for OCT-1 revealed two band shifts in cells on polyHEMA with cAMP and on EHS-drip, which were repressed by the GJIC inhibitor, 18α-GA. These studies demonstrated that mammary cells on polyHEMA expressed β-casein in response to prolactin in a pathway that involves GJIC and OCT-1 and is independent of STAT5 nuclear translocation.</p>\",\"PeriodicalId\":55269,\"journal\":{\"name\":\"Cell Communication and Adhesion\",\"volume\":\"18 5\",\"pages\":\"104-16\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2011-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.3109/15419061.2011.639468\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cell Communication and Adhesion\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3109/15419061.2011.639468\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2011/12/5 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"Biochemistry, Genetics and Molecular Biology\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Communication and Adhesion","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3109/15419061.2011.639468","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2011/12/5 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
Gap junctions mediate STAT5-independent β-casein expression in CID-9 mammary epithelial cells.
Crosstalk between gap junction intracellular communication (GJIC), STAT5 and OCT-1 in gap junction (GJ)-dependent β-casein expression was investigated. CID-9 mammary cells plated with prolactin on non-adherent substratum (poly-HEMA) expressed β-casein independent of STAT5 only in the presence of the GJIC inducer, cAMP. Nuclear STAT5 levels were not detectable. By contrast, cells on EHS-drip expressed β-casein in a STAT5-dependent manner and nuclear STAT5 levels were up-regulated. A 75 kDa OCT-1 isoform was detected in conditions that induced β-casein expression regardless of substratum. Interestingly, 40 and 28 kDa OCT-1 isoforms were induced in cells on polyHEMA with cAMP. Electrophoretic mobility shift assays (EMSA) for OCT-1 revealed two band shifts in cells on polyHEMA with cAMP and on EHS-drip, which were repressed by the GJIC inhibitor, 18α-GA. These studies demonstrated that mammary cells on polyHEMA expressed β-casein in response to prolactin in a pathway that involves GJIC and OCT-1 and is independent of STAT5 nuclear translocation.
期刊介绍：
Cessation
Cell Communication and Adhesion is an international Open Access journal which provides a central forum for research on mechanisms underlying cellular signalling and adhesion. The journal provides a single source of information concerning all forms of cellular communication, cell junctions, adhesion molecules and families of receptors from diverse biological systems.
The journal welcomes submission of original research articles, reviews, short communications and conference reports.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
