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http://purl.uniprot.org/citations/28732559http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28732559http://www.w3.org/2000/01/rdf-schema#comment"Tumor necrosis factor-α (TNF-α) is suggested to induce mitochondrial dysfunction and apoptosis of renal tubular epithelial cells that possibly exacerbates renal function in chronic kidney disease (CKD). Here we investigated whether suppressor of cytokine signaling-1 (SOCS-1), an inhibitor of cytokine signaling, was involved in TNF-α-induced human renal tubular epithelial cells (HKCs) oxidative stress and apoptosis. TNF-α promoted the protein and mRNA expression of SOCS-1 in a time and dose dependent manner, along with increased cell apoptosis and activation of apoptosis signal regulating kinase-1(ASK1) in HKCs. Furthermore, overexpression of SOCS-1 in HKCs reduced TNF-α-mediated oxidative stress and apoptosis. Meanwhile, We also found that overexpression of SOCS-1 could regulate the activity of JAK/STAT signaling pathway. In addition, a specific JAK2 inhibitor, AG490, that both attenuated TNF-α-induced oxidative stress, also reduced apoptosis. Taken together, overexpression of SOCS-1 prevented TNF-α-mediated cell oxidative stress and apoptosis may be via suppression of JAK/STAT signaling pathway activation in HKCs."xsd:string
http://purl.uniprot.org/citations/28732559http://purl.org/dc/terms/identifier"doi:10.1016/j.tice.2017.06.005"xsd:string
http://purl.uniprot.org/citations/28732559http://purl.uniprot.org/core/author"Du Y."xsd:string
http://purl.uniprot.org/citations/28732559http://purl.uniprot.org/core/author"Ren Y."xsd:string
http://purl.uniprot.org/citations/28732559http://purl.uniprot.org/core/author"Shi Y."xsd:string
http://purl.uniprot.org/citations/28732559http://purl.uniprot.org/core/author"Wu H."xsd:string
http://purl.uniprot.org/citations/28732559http://purl.uniprot.org/core/author"Wei J."xsd:string
http://purl.uniprot.org/citations/28732559http://purl.uniprot.org/core/author"Yao F."xsd:string
http://purl.uniprot.org/citations/28732559http://purl.uniprot.org/core/author"Duan H."xsd:string
http://purl.uniprot.org/citations/28732559http://purl.uniprot.org/core/author"Du C."xsd:string
http://purl.uniprot.org/citations/28732559http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/28732559http://purl.uniprot.org/core/name"Tissue Cell"xsd:string
http://purl.uniprot.org/citations/28732559http://purl.uniprot.org/core/pages"537-544"xsd:string
http://purl.uniprot.org/citations/28732559http://purl.uniprot.org/core/title"SOCS-1 is involved in TNF-alpha-induced mitochondrial dysfunction and apoptosis in renal tubular epithelial cells."xsd:string
http://purl.uniprot.org/citations/28732559http://purl.uniprot.org/core/volume"49"xsd:string
http://purl.uniprot.org/citations/28732559http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/28732559
http://purl.uniprot.org/citations/28732559http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/28732559
http://purl.uniprot.org/uniprot/#_O15524-mappedCitation-28732559http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28732559
http://purl.uniprot.org/uniprot/#_Q4JHT5-mappedCitation-28732559http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28732559
http://purl.uniprot.org/uniprot/O15524http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/28732559
http://purl.uniprot.org/uniprot/Q4JHT5http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/28732559