http://purl.uniprot.org/citations/15677458 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/15677458 | http://www.w3.org/2000/01/rdf-schema#comment | "The transforming growth factor-beta (TGF-beta) family of secreted proteins have pleiotropic functions that are critical to normal development and homeostasis. However, the intracellular mechanisms by which the TGF-beta proteins elicit cellular responses remain incompletely understood. The Smad proteins provide a major means for the propagation of the TGF-beta signal from the cell surface to the nucleus, where the Smad proteins regulate gene expression leading to TGF-beta-dependent cellular responses including the inhibition of cell proliferation. Recent studies have suggested that a nuclear Smad-interacting protein termed SnoN, when overexpressed in cells, suppresses TGF-beta-induced Smad signaling and TGF-beta inhibition of cell proliferation. However, the physiologic function of endogenous SnoN in TGF-beta-mediated biological responses remained to be elucidated. Here, we determined the effect of genetic knock-down of SnoN by RNA interference on TGF-beta responses in mammalian cells. Unexpectedly, we found that SnoN knock-down specifically inhibited TGF-beta-induced transcription in the lung epithelial cell line Mv1Lu but not in HeLa or HaCaT cells. SnoN knock-down was also found to block TGF-beta-dependent cell cycle arrest in Mv1Lu cells. Collectively, these data indicate that rather than suppressing TGF-beta-induced responses, endogenous SnoN acts as a positive mediator of TGF-beta-induced transcription and cell cycle arrest in lung epithelial cells. Our study also shows that SnoN couples the TGF-beta signal to gene expression in a cell-specific manner."xsd:string |
http://purl.uniprot.org/citations/15677458 | http://purl.org/dc/terms/identifier | "doi:10.1074/jbc.m409367200"xsd:string |
http://purl.uniprot.org/citations/15677458 | http://purl.uniprot.org/core/author | "Wilson S.M."xsd:string |
http://purl.uniprot.org/citations/15677458 | http://purl.uniprot.org/core/author | "Bonni S."xsd:string |
http://purl.uniprot.org/citations/15677458 | http://purl.uniprot.org/core/author | "Sarker K.P."xsd:string |
http://purl.uniprot.org/citations/15677458 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
http://purl.uniprot.org/citations/15677458 | http://purl.uniprot.org/core/name | "J Biol Chem"xsd:string |
http://purl.uniprot.org/citations/15677458 | http://purl.uniprot.org/core/pages | "13037-13046"xsd:string |
http://purl.uniprot.org/citations/15677458 | http://purl.uniprot.org/core/title | "SnoN is a cell type-specific mediator of transforming growth factor-beta responses."xsd:string |
http://purl.uniprot.org/citations/15677458 | http://purl.uniprot.org/core/volume | "280"xsd:string |
http://purl.uniprot.org/citations/15677458 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/15677458 |
http://purl.uniprot.org/citations/15677458 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/15677458 |
http://purl.uniprot.org/uniprot/#_I6QMM9-mappedCitation-15677458 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15677458 |
http://purl.uniprot.org/uniprot/#_P12757-mappedCitation-15677458 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/15677458 |
http://purl.uniprot.org/uniprot/P12757 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/15677458 |
http://purl.uniprot.org/uniprot/I6QMM9 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/15677458 |