Matches in SemOpenAlex for { <https://semopenalex.org/work/W2089383992> ?p ?o ?g. }
- W2089383992 endingPage "545" @default.
- W2089383992 startingPage "538" @default.
- W2089383992 abstract "Shear stress-induced extracellular signal-regulated kinase (ERK)5 activation and the consequent regulation of Kruppel-like factor 2 and endothelial nitric oxide synthase expression represents one of the antiinflammatory and vascular tone regulatory mechanisms maintaining normal endothelial function. Endothelial dysfunction is a major initiator of atherosclerosis, a vascular pathology often associated with diabetes. Small ubiquitin-like modifier (SUMO) covalently attaches to certain residues of specific target transcription factors and could inhibit its activity. We investigated whether H(2)O(2) and AGE (advanced glycation end products), 2 well-known mediators of diabetes, negatively regulated ERK5 transcriptional activity and laminar flow-induced endothelial nitric oxide synthase expression through ERK5 SUMOylation. H(2)O(2) and AGE induced endogenous ERK5 SUMOylation. In addition, ERK5 SUMOylation was increased in the aortas from diabetic mice. ERK5 transcriptional activity, but not kinase activity, was inhibited by expression of Ubc9 (SUMO E2 conjugase) or PIAS1 (E3 ligase), suggesting the involvement of ERK5 SUMOylation on its transcriptional activity. Point-mutation analyses showed that ERK5 is covalently modified by SUMO at 2 conserved sites, Lys6 and Lys22, and that the SUMOylation defective mutant of ERK5, dominant negative form of Ubc9 (DN-Ubc9), and small interfering RNA PIAS1 reversed H(2)O(2) and AGE-mediated reduction of shear stress-mediated ERK5/myocyte enhancer factor 2 transcriptional activity, as well as promoter activity of Kruppel-like factor 2. Finally, PIAS1 knockdown reversed the inhibitory effect of H(2)O(2) in shear stress-induced Kruppel-like factor 2 and endothelial nitric oxide synthase expression. These data clearly defined SUMOylation-dependent ERK5 transcriptional repression independent of kinase activity and suggested this process as among the molecular mechanisms of diabetes-mediated endothelial dysfunction." @default.
- W2089383992 created "2016-06-24" @default.
- W2089383992 creator A5024589429 @default.
- W2089383992 creator A5034101987 @default.
- W2089383992 creator A5037470341 @default.
- W2089383992 creator A5044778439 @default.
- W2089383992 creator A5055245284 @default.
- W2089383992 creator A5056395040 @default.
- W2089383992 creator A5064765788 @default.
- W2089383992 creator A5066931963 @default.
- W2089383992 date "2008-03-14" @default.
- W2089383992 modified "2023-09-25" @default.
- W2089383992 title "Extracellular Signal-Regulated Kinase 5 SUMOylation Antagonizes Shear Stress–Induced Antiinflammatory Response and Endothelial Nitric Oxide Synthase Expression in Endothelial Cells" @default.
- W2089383992 cites W1744223828 @default.
- W2089383992 cites W1884928119 @default.
- W2089383992 cites W1975974235 @default.
- W2089383992 cites W1991972495 @default.
- W2089383992 cites W1992125440 @default.
- W2089383992 cites W1998607972 @default.
- W2089383992 cites W2004722555 @default.
- W2089383992 cites W2011080190 @default.
- W2089383992 cites W2033209518 @default.
- W2089383992 cites W2036455976 @default.
- W2089383992 cites W2037792829 @default.
- W2089383992 cites W2045893413 @default.
- W2089383992 cites W2056596114 @default.
- W2089383992 cites W2068856879 @default.
- W2089383992 cites W2070182263 @default.
- W2089383992 cites W2073714833 @default.
- W2089383992 cites W2079753883 @default.
- W2089383992 cites W2082502030 @default.
- W2089383992 cites W2084030324 @default.
- W2089383992 cites W2089674453 @default.
- W2089383992 cites W2104079111 @default.
- W2089383992 cites W2112441454 @default.
- W2089383992 cites W2122044343 @default.
- W2089383992 cites W2122575066 @default.
- W2089383992 cites W2129103503 @default.
- W2089383992 cites W2132740540 @default.
- W2089383992 cites W2133546870 @default.
- W2089383992 cites W2134450450 @default.
- W2089383992 cites W2134468110 @default.
- W2089383992 cites W2146234609 @default.
- W2089383992 cites W2147919276 @default.
- W2089383992 cites W2154075930 @default.
- W2089383992 cites W4231082968 @default.
- W2089383992 doi "https://doi.org/10.1161/circresaha.107.156877" @default.
- W2089383992 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18218985" @default.
- W2089383992 hasPublicationYear "2008" @default.
- W2089383992 type Work @default.
- W2089383992 sameAs 2089383992 @default.
- W2089383992 citedByCount "110" @default.
- W2089383992 countsByYear W20893839922012 @default.
- W2089383992 countsByYear W20893839922013 @default.
- W2089383992 countsByYear W20893839922014 @default.
- W2089383992 countsByYear W20893839922015 @default.
- W2089383992 countsByYear W20893839922016 @default.
- W2089383992 countsByYear W20893839922017 @default.
- W2089383992 countsByYear W20893839922018 @default.
- W2089383992 countsByYear W20893839922019 @default.
- W2089383992 countsByYear W20893839922020 @default.
- W2089383992 countsByYear W20893839922021 @default.
- W2089383992 countsByYear W20893839922022 @default.
- W2089383992 countsByYear W20893839922023 @default.
- W2089383992 crossrefType "journal-article" @default.
- W2089383992 hasAuthorship W2089383992A5024589429 @default.
- W2089383992 hasAuthorship W2089383992A5034101987 @default.
- W2089383992 hasAuthorship W2089383992A5037470341 @default.
- W2089383992 hasAuthorship W2089383992A5044778439 @default.
- W2089383992 hasAuthorship W2089383992A5055245284 @default.
- W2089383992 hasAuthorship W2089383992A5056395040 @default.
- W2089383992 hasAuthorship W2089383992A5064765788 @default.
- W2089383992 hasAuthorship W2089383992A5066931963 @default.
- W2089383992 hasBestOaLocation W20893839921 @default.
- W2089383992 hasConcept C104317684 @default.
- W2089383992 hasConcept C134459356 @default.
- W2089383992 hasConcept C153911025 @default.
- W2089383992 hasConcept C171350616 @default.
- W2089383992 hasConcept C178790620 @default.
- W2089383992 hasConcept C181199279 @default.
- W2089383992 hasConcept C185592680 @default.
- W2089383992 hasConcept C22615655 @default.
- W2089383992 hasConcept C25602115 @default.
- W2089383992 hasConcept C2776015013 @default.
- W2089383992 hasConcept C2777622882 @default.
- W2089383992 hasConcept C519581460 @default.
- W2089383992 hasConcept C538909803 @default.
- W2089383992 hasConcept C54009773 @default.
- W2089383992 hasConcept C55493867 @default.
- W2089383992 hasConcept C57074206 @default.
- W2089383992 hasConcept C62478195 @default.
- W2089383992 hasConcept C86339819 @default.
- W2089383992 hasConcept C86803240 @default.
- W2089383992 hasConcept C95444343 @default.
- W2089383992 hasConceptScore W2089383992C104317684 @default.
- W2089383992 hasConceptScore W2089383992C134459356 @default.
- W2089383992 hasConceptScore W2089383992C153911025 @default.
- W2089383992 hasConceptScore W2089383992C171350616 @default.