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http://purl.uniprot.org/citations/23024367http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23024367http://www.w3.org/2000/01/rdf-schema#comment"Pro-tumorigenic function of the p38 kinase plays a critical role in human cholangiocarcinogenesis. However, the underlying mechanism remains incompletely understood. Here, we report that c-Met, the tyrosine kinase receptor for hepatocyte growth factor (HGF), contributes to the pro-tumorigenic ability of p38 in human cholangiocarcinoma cells. Both p38 and c-Met promote the proliferation and invasion of human cholangiocarcinoma cells. Importantly, inhibition or knockdown of p38 decreased the basal activation of c-Met. Tyrosine phosphatase inhibitor studies revealed that p38 promotes the activity of c-Met, at least in part, by inhibiting dephosphorylation of the receptor. Moreover, density enhanced phosphatase-1 (DEP-1) is involved in p38-mediated inhibiting dephosphorylation of c-Met. Furthermore, p38 inhibits the degradation of c-Met. Taken together, these data provide a potential mechanism to explain how p38 promotes human cholangiocarcinoma cell proliferation and invasion. We propose that the link between p38 and c-Met is implicated in the progression of human cholangiocarcinoma."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m112.406520"xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/author"Dai R."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/author"Chen Y."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/author"Cao J."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/author"Li N."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/author"Qian Y."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/author"Ren Y."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/author"Wang H."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/author"Zhao X."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/author"Zhu J."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/author"Wang R."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/author"Fu J."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/author"Luo T."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/name"J Biol Chem"xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/pages"39812-39823"xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/title"The tyrosine kinase c-Met contributes to the pro-tumorigenic function of the p38 kinase in human bile duct cholangiocarcinoma cells."xsd:string
http://purl.uniprot.org/citations/23024367http://purl.uniprot.org/core/volume"287"xsd:string
http://purl.uniprot.org/citations/23024367http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23024367
http://purl.uniprot.org/citations/23024367http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23024367
http://purl.uniprot.org/uniprot/#_A5D6Q9-mappedCitation-23024367http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23024367
http://purl.uniprot.org/uniprot/#_A0A510GDE6-mappedCitation-23024367http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23024367