File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: PIKE-A is required for prolactin-mediated STAT5a activation in mammary gland development

TitlePIKE-A is required for prolactin-mediated STAT5a activation in mammary gland development
Authors
KeywordsMammary gland
PIKE
STAT5
Prolactin receptor
Issue Date2010
Citation
EMBO Journal, 2010, v. 29, n. 5, p. 956-968 How to Cite?
AbstractPI 3-kinase enhancer A (PIKE-A) is critical for the activation of Akt signalling, and has an essential function in promoting cancer cell survival. However, its physiological functions are poorly understood. Here, we show that PIKE-A directly associates with both signal transducer and activator of transcription 5a (STAT5a) and prolactin (PRL) receptor, which is essential for PRL-provoked STAT5a activation and the subsequent gene transcription. Depletion of PIKE-A in HC11 epithelial cells diminished PRL-induced STAT5 activation and cyclin D1 expression, resulting in profoundly impaired cell proliferation in vitro. To confirm the function of PIKE-A in PRL signalling in vivo, we generated PIKE knockout (PIKE/) mice. PIKE/ mice displayed a severe lactation defect that was characterized by enhanced apoptosis and impaired proliferation of mammary epithelial cells. At parturition, STAT5 activation and cyclin D1 expression were substantially reduced in the mammary epithelium of PIKE/ mice. The defective mammary gland development in PIKE/ mice was rescued by overexpression of a mammary-specific cyclin D1 transgene. These data establish a critical function for PIKE-A in mediating PRL functions. © 2010 European Molecular Biology Organization | All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/225081
ISSN
2015 Impact Factor: 9.643
2015 SCImago Journal Rankings: 7.450

 

DC FieldValueLanguage
dc.contributor.authorChan, Chi B.-
dc.contributor.authorLiu, Xia-
dc.contributor.authorEnsslin, Michael A.-
dc.contributor.authorDillehay, Dirck L.-
dc.contributor.authorOrmandy, Christopher J.-
dc.contributor.authorSohn, Philip-
dc.contributor.authorSerra, Rosa-
dc.contributor.authorYe, Keqiang-
dc.date.accessioned2016-04-18T11:16:43Z-
dc.date.available2016-04-18T11:16:43Z-
dc.date.issued2010-
dc.identifier.citationEMBO Journal, 2010, v. 29, n. 5, p. 956-968-
dc.identifier.issn0261-4189-
dc.identifier.urihttp://hdl.handle.net/10722/225081-
dc.description.abstractPI 3-kinase enhancer A (PIKE-A) is critical for the activation of Akt signalling, and has an essential function in promoting cancer cell survival. However, its physiological functions are poorly understood. Here, we show that PIKE-A directly associates with both signal transducer and activator of transcription 5a (STAT5a) and prolactin (PRL) receptor, which is essential for PRL-provoked STAT5a activation and the subsequent gene transcription. Depletion of PIKE-A in HC11 epithelial cells diminished PRL-induced STAT5 activation and cyclin D1 expression, resulting in profoundly impaired cell proliferation in vitro. To confirm the function of PIKE-A in PRL signalling in vivo, we generated PIKE knockout (PIKE/) mice. PIKE/ mice displayed a severe lactation defect that was characterized by enhanced apoptosis and impaired proliferation of mammary epithelial cells. At parturition, STAT5 activation and cyclin D1 expression were substantially reduced in the mammary epithelium of PIKE/ mice. The defective mammary gland development in PIKE/ mice was rescued by overexpression of a mammary-specific cyclin D1 transgene. These data establish a critical function for PIKE-A in mediating PRL functions. © 2010 European Molecular Biology Organization | All Rights Reserved.-
dc.languageeng-
dc.relation.ispartofEMBO Journal-
dc.subjectMammary gland-
dc.subjectPIKE-
dc.subjectSTAT5-
dc.subjectProlactin receptor-
dc.titlePIKE-A is required for prolactin-mediated STAT5a activation in mammary gland development-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1038/emboj.2009.406-
dc.identifier.pmid20075866-
dc.identifier.scopuseid_2-s2.0-77649341620-
dc.identifier.volume29-
dc.identifier.issue5-
dc.identifier.spage956-
dc.identifier.epage968-
dc.identifier.eissn1460-2075-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats