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http://purl.uniprot.org/citations/25375133http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25375133http://www.w3.org/2000/01/rdf-schema#comment"Niacin has been demonstrated to activate a PI3K/Akt signaling cascade to prevent brain damage after stroke and UV-induced skin damage; however, the underlying molecular mechanisms for HCA2-induced Akt activation remain to be elucidated. Using CHO-K1 cells stably expressing HCA2 and A431 cells, a human epidermoid cell line with high levels of endogenous expression of functional HCA2 receptors, we first demonstrated that niacin induced a robust Akt phosphorylation at both Thr308 and Ser473 in a time-dependent fashion, with a maximal activation at 5 min and a subsequent reduction to baseline by 30 min through HCA2, and that the activation was significantly blocked by pertussis toxin. The HCA2-mediated activation of Akt was also significantly inhibited by the PKC inhibitors GF109203x and Go6983 in both cell lines, by the PDGFR-selective inhibitor tyrphostin A9 in CHO-HCA2 cells and by the MMP inhibitor GM6001 and EGFR-specific inhibitor AG1478 in A431 cells. These results suggest that the PKC pathway and PDGFR/EGFR transactivation pathway play important roles in HCA2-mediated Akt activation. Further investigation indicated that PI3K and the Gβγ subunit were likely to play an essential role in HCA2-induced Akt activation. Moreover, Immunobloting analyses using an antibody that recognizes p70S6K1 phosphorylated at Thr389 showed that niacin evoked p70S6K1 activation via the PI3K/Akt pathway. The results of our study provide new insight into the signaling pathways involved in HCA2 activation."xsd:string
http://purl.uniprot.org/citations/25375133http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0112310"xsd:string
http://purl.uniprot.org/citations/25375133http://purl.uniprot.org/core/author"Lu J."xsd:string
http://purl.uniprot.org/citations/25375133http://purl.uniprot.org/core/author"Li G."xsd:string
http://purl.uniprot.org/citations/25375133http://purl.uniprot.org/core/author"Sun H."xsd:string
http://purl.uniprot.org/citations/25375133http://purl.uniprot.org/core/author"Shi Y."xsd:string
http://purl.uniprot.org/citations/25375133http://purl.uniprot.org/core/author"Zhang W."xsd:string
http://purl.uniprot.org/citations/25375133http://purl.uniprot.org/core/author"Yu Y."xsd:string
http://purl.uniprot.org/citations/25375133http://purl.uniprot.org/core/author"Zhou Q."xsd:string
http://purl.uniprot.org/citations/25375133http://purl.uniprot.org/core/author"Zhou N."xsd:string
http://purl.uniprot.org/citations/25375133http://purl.uniprot.org/core/author"Offermanns S."xsd:string
http://purl.uniprot.org/citations/25375133http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/25375133http://purl.uniprot.org/core/name"PLoS One"xsd:string
http://purl.uniprot.org/citations/25375133http://purl.uniprot.org/core/pages"e112310"xsd:string
http://purl.uniprot.org/citations/25375133http://purl.uniprot.org/core/title"Niacin activates the PI3K/Akt cascade via PKC- and EGFR-transactivation-dependent pathways through hydroxyl-carboxylic acid receptor 2."xsd:string
http://purl.uniprot.org/citations/25375133http://purl.uniprot.org/core/volume"9"xsd:string
http://purl.uniprot.org/citations/25375133http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25375133
http://purl.uniprot.org/citations/25375133http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25375133
http://purl.uniprot.org/uniprot/#_D3Z783-mappedCitation-25375133http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25375133
http://purl.uniprot.org/uniprot/#_A0A068JD88-mappedCitation-25375133http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25375133
http://purl.uniprot.org/uniprot/#_A8K2T7-mappedCitation-25375133http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25375133
http://purl.uniprot.org/uniprot/#_A0A068JCC9-mappedCitation-25375133http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25375133
http://purl.uniprot.org/uniprot/#_A0A1Y0B9F8-mappedCitation-25375133http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25375133
http://purl.uniprot.org/uniprot/#_D3YYP9-mappedCitation-25375133http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25375133