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http://purl.uniprot.org/citations/30562745http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/30562745http://www.w3.org/2000/01/rdf-schema#comment"

Background/aims

Chronic inflammation contributes to the development of type 2 diabetes mellitus by targeting the insulin receptor substrate protein-1 (IRS-1) signaling pathway. Previous studies showed that Leukemia related protein 16 (LRP16) reduced insulin stimulated glucose uptake in adipocytes by impairing the IRS-1 signaling pathway. We explored the mechanism by which LRP16 promotes the inflammatory response.

Methods

We screened LRP16 induced proteins in the lipopolysaccharide (LPS)-stimulated inflammatory response using liquid chromatography-mass spectrometry (LC-MS) and analyzed the potential biological functions of these proteins using online bioinformatics tools. mRNA expression and protein expression of target genes were measured by real time PCR and Western blot, respectively.

Results

A total of 390 differentially expressed proteins were identified. The mitogen-activated protein kinase (MAPK) signaling pathway was the primary activated pathway in LRP16-expressing cells. Overexpression of LRP16 activated ERK1/2 and Rac1, which are two key players related to the MAPK signaling pathway. Furthermore, knock down of endogenous LRP16 by RNA interference (RNAi) reduced Rac1 expression, ERK activation, and inflammatory cytokine expression in human adipocytes stimulated by LPS. The stimulatory effect of LRP16 was diminished by suppressing Rac1 expression and treating the cells with the ERK specific inhibitor, PD98059.

Conclusion

These findings revealed the functions of LRP16 in promoting the inflammatory response through activating the Rac1-MAPK1/ERK pathway in human adipocytes."xsd:string
http://purl.uniprot.org/citations/30562745http://purl.org/dc/terms/identifier"doi:10.1159/000495931"xsd:string
http://purl.uniprot.org/citations/30562745http://purl.uniprot.org/core/author"Gu W."xsd:string
http://purl.uniprot.org/citations/30562745http://purl.uniprot.org/core/author"Lyu Z."xsd:string
http://purl.uniprot.org/citations/30562745http://purl.uniprot.org/core/author"Wu D."xsd:string
http://purl.uniprot.org/citations/30562745http://purl.uniprot.org/core/author"Yang G."xsd:string
http://purl.uniprot.org/citations/30562745http://purl.uniprot.org/core/author"Wang A."xsd:string
http://purl.uniprot.org/citations/30562745http://purl.uniprot.org/core/author"Zang L."xsd:string
http://purl.uniprot.org/citations/30562745http://purl.uniprot.org/core/author"Mu Y."xsd:string
http://purl.uniprot.org/citations/30562745http://purl.uniprot.org/core/author"Hong Q."xsd:string
http://purl.uniprot.org/citations/30562745http://purl.uniprot.org/core/author"Dou J."xsd:string
http://purl.uniprot.org/citations/30562745http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/30562745http://purl.uniprot.org/core/name"Cell Physiol Biochem"xsd:string
http://purl.uniprot.org/citations/30562745http://purl.uniprot.org/core/pages"2591-2603"xsd:string
http://purl.uniprot.org/citations/30562745http://purl.uniprot.org/core/title"MACROD1/LRP16 Enhances LPS-Stimulated Inflammatory Responses by Up-Regulating a Rac1-Dependent Pathway in Adipocytes."xsd:string
http://purl.uniprot.org/citations/30562745http://purl.uniprot.org/core/volume"51"xsd:string
http://purl.uniprot.org/citations/30562745http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/30562745
http://purl.uniprot.org/citations/30562745http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/30562745
http://purl.uniprot.org/uniprot/#_Q9BQ69-mappedCitation-30562745http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30562745
http://purl.uniprot.org/uniprot/Q9BQ69http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/30562745