| http://purl.uniprot.org/citations/15976007 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15976007 | http://www.w3.org/2000/01/rdf-schema#comment | "CRH-binding protein (CRH-BP) binds CRH with high affinity and inhibits CRH-mediated ACTH release from anterior pituitary corticotrope-like cells in vitro. In female mouse pituitary, CRH-BP is localized not only in corticotropes, but is also expressed in gonadotropes and lactotropes. To investigate the functional significance of gonadotrope CRH-BP, we examined the molecular mechanisms underlying GnRH-regulated CRH-BP expression in alphaT3-1 gonadotrope-like cells. CRH-BP is endogenously expressed in alphaT3-1 cells, and quantitative real-time RT-PCR and ribonuclease protection assays demonstrate that GnRH induces a 3.7-fold increase in CRH-BP mRNA levels. GnRH also induces intracellular CRH-BP (2.0-fold) and secreted CRH-BP (5.3-fold) levels, as measured by [125I]CRH:CRH-BP chemical cross-linking. Transient transfection assays using CRH-BP promoter-luciferase constructs indicate that GnRH regulation involves protein kinase C-, ERK- and calcium-dependent signaling pathways and is mediated via a multipartite GnRH response element that includes activator protein 1 and cAMP response element (CRE) sites. The CRE site significantly contributes to GnRH responsiveness, independent of protein kinase A, representing a unique form of multipartite GnRH regulation in alphaT3-1 cells. Furthermore, EMSAs indicate that alphaT3-1 nuclear proteins specifically bind at activator protein 1 and CRE sites. These data demonstrate novel regulation of pituitary CRH-BP, highlighting the importance of the pituitary gonadotrope as a potential interface between the stress and reproductive axes."xsd:string |
| http://purl.uniprot.org/citations/15976007 | http://purl.org/dc/terms/identifier | "doi:10.1210/me.2004-0519"xsd:string |
| http://purl.uniprot.org/citations/15976007 | http://purl.uniprot.org/core/author | "Seasholtz A.F."xsd:string |
| http://purl.uniprot.org/citations/15976007 | http://purl.uniprot.org/core/author | "Westphal N.J."xsd:string |
| http://purl.uniprot.org/citations/15976007 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
| http://purl.uniprot.org/citations/15976007 | http://purl.uniprot.org/core/name | "Mol Endocrinol"xsd:string |
| http://purl.uniprot.org/citations/15976007 | http://purl.uniprot.org/core/pages | "2780-2797"xsd:string |
| http://purl.uniprot.org/citations/15976007 | http://purl.uniprot.org/core/title | "Gonadotropin-releasing hormone (GnRH) positively regulates corticotropin-releasing hormone-binding protein expression via multiple intracellular signaling pathways and a multipartite GnRH response element in alphaT3-1 cells."xsd:string |
| http://purl.uniprot.org/citations/15976007 | http://purl.uniprot.org/core/volume | "19"xsd:string |
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