| http://purl.uniprot.org/citations/7969170 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/7969170 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/7969170 | http://www.w3.org/2000/01/rdf-schema#comment | "The biological response to progesterone is mediated by two distinct forms of the human progesterone receptor (hPR-A and hPR-B). In most cell contexts, hPR-B functions as a transcriptional activator of progesterone-responsive genes, whereas hPR-A functions as a transcriptional inhibitor of all steroid hormone receptors. We have created mutations within the carboxyl terminus of hPR which differentially effect the transcriptional activity of hPR-B in a cell- and promoter-specific manner. Analogous mutations, when introduced into hPR-A, have no effect on its ability to inhibit the transcriptional activity of other steroid hormone receptors. The observed differences in the structural requirements for hPR-B and hPR-A function suggest that transcriptional activation and repression by PR are mediated by two separate pathways within the cell. In support of this hypothesis, we have shown that hPR-A mediated repression of human estrogen receptor (hER) transcriptional activity is not dependent on hER expression level but depends largely on the absolute expression level of hPR-A. Thus, it appears that hPR-A inhibits hER transcriptional activity as a consequence of a noncompetitive interaction of hPR-A with either distinct cellular targets or different contact sites on the same target. We propose that hPR-A expression facilitates a ligand-dependent cross-talk among sex steroid receptor signaling pathways within the cell. It is likely, therefore, that alterations in the expression level of hPR-A or its cellular target can have profound effects on the physiological or pharmacological responses to sex steroid hormone receptor ligands."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.org/dc/terms/identifier | "doi:10.1128/mcb.14.12.8356-8364.1994"xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.org/dc/terms/identifier | "doi:10.1128/mcb.14.12.8356-8364.1994"xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/author | "Xu Y.F."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/author | "Xu Y.F."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/author | "McDonnell D.P."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/author | "McDonnell D.P."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/author | "Goldman M.E."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/author | "Goldman M.E."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/author | "Mais D.E."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/author | "Mais D.E."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/author | "Wen D.X."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/author | "Wen D.X."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/date | "1994"xsd:gYear |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/date | "1994"xsd:gYear |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/name | "Mol. Cell. Biol."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/name | "Mol. Cell. Biol."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/pages | "8356-8364"xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/pages | "8356-8364"xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/title | "The A and B isoforms of the human progesterone receptor operate through distinct signaling pathways within target cells."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/title | "The A and B isoforms of the human progesterone receptor operate through distinct signaling pathways within target cells."xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/volume | "14"xsd:string |
| http://purl.uniprot.org/citations/7969170 | http://purl.uniprot.org/core/volume | "14"xsd:string |