| http://purl.uniprot.org/citations/23085260 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/23085260 | http://www.w3.org/2000/01/rdf-schema#comment | "Hyperglycemia-induced endothelial dysfunction is characterized by enhanced inflammatory cytokine and adhesion molecule expression, and endothelial-monocyte adhesion. The adapter molecule CIKS (connection to IKK and SAPK/JNK; also known as Act1 or TRAF3IP2) is an upstream regulator of NF-κB and AP-1, and plays a role in inflammation and injury. Here we show that high glucose (HG; 25mM vs. 5mM d-glucose)-induced endothelial-monocyte adhesion and inhibition of endothelial cell (EC) migration were both reversed by CIKS knockdown. In EC, HG induced CIKS mRNA and protein expression via DPI-inhibitable Nox4-dependent ROS generation. Further, HG induced CIKS transcription and enhanced CIKS promoter-dependent reporter gene activation via Nox4, ROS, AP-1 and C/EBP. Coimmunoprecipitation and immunoblotting revealed CIKS/IKKβ/JNK physical association under basal conditions that was enhanced by HG treatment. Importantly, CIKS knockdown inhibited HG-induced (i) IKKβ and JNK phosphorylation, (ii) p65 and c-Jun nuclear translocation, and (iii) NF-κB- and AP-1-dependent proinflammatory cytokine, chemokine, and adhesion molecule expression. Similar to HG, the deleterious metabolic products of chronic hyperglycemia, AGE-HSA, AOPPs-HSA and oxLDL, also induced CIKS-dependent endothelial dysfunction. Notably, aortas from streptozotocin-induced and the autoimmune type 1 diabetic NOD and Akita mice showed enhanced DPI-inhibitable ROS generation and CIKS expression. Since CIKS mediates high glucose-induced NF-κB and AP-1-dependent inflammatory signaling and endothelial dysfunction, targeting CIKS may delay progression of vascular diseases during diabetes mellitus and atherosclerosis."xsd:string |
| http://purl.uniprot.org/citations/23085260 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.cellsig.2012.10.009"xsd:string |
| http://purl.uniprot.org/citations/23085260 | http://purl.uniprot.org/core/author | "Yoshida T."xsd:string |
| http://purl.uniprot.org/citations/23085260 | http://purl.uniprot.org/core/author | "Siebenlist U."xsd:string |
| http://purl.uniprot.org/citations/23085260 | http://purl.uniprot.org/core/author | "Valente A.J."xsd:string |
| http://purl.uniprot.org/citations/23085260 | http://purl.uniprot.org/core/author | "Chandrasekar B."xsd:string |
| http://purl.uniprot.org/citations/23085260 | http://purl.uniprot.org/core/author | "Carpenter A.J."xsd:string |
| http://purl.uniprot.org/citations/23085260 | http://purl.uniprot.org/core/author | "Venkatesan B."xsd:string |
| http://purl.uniprot.org/citations/23085260 | http://purl.uniprot.org/core/author | "Das N.A."xsd:string |
| http://purl.uniprot.org/citations/23085260 | http://purl.uniprot.org/core/author | "Delafontaine J.L."xsd:string |
| http://purl.uniprot.org/citations/23085260 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
| http://purl.uniprot.org/citations/23085260 | http://purl.uniprot.org/core/name | "Cell Signal"xsd:string |
| http://purl.uniprot.org/citations/23085260 | http://purl.uniprot.org/core/pages | "359-371"xsd:string |
| http://purl.uniprot.org/citations/23085260 | http://purl.uniprot.org/core/title | "CIKS (Act1 or TRAF3IP2) mediates high glucose-induced endothelial dysfunction."xsd:string |
| http://purl.uniprot.org/citations/23085260 | http://purl.uniprot.org/core/volume | "25"xsd:string |
| http://purl.uniprot.org/citations/23085260 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/23085260 |
| http://purl.uniprot.org/citations/23085260 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/23085260 |
| http://purl.uniprot.org/uniprot/#_I7GPR1-mappedCitation-23085260 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23085260 |
| http://purl.uniprot.org/uniprot/#_I7GPT0-mappedCitation-23085260 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23085260 |
| http://purl.uniprot.org/uniprot/#_Q6IR26-mappedCitation-23085260 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23085260 |
| http://purl.uniprot.org/uniprot/#_Q8N7N6-mappedCitation-23085260 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23085260 |
| http://purl.uniprot.org/uniprot/#_Q8R227-mappedCitation-23085260 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23085260 |
| http://purl.uniprot.org/uniprot/#_Q8C0E5-mappedCitation-23085260 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/23085260 |
| http://purl.uniprot.org/uniprot/Q8N7N6 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/23085260 |