FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2022846817> ?p ?o ?g. }

• W2022846817 endingPage "99" @default.
• W2022846817 startingPage "90" @default.
• W2022846817 abstract "Cardiac hypertrophy is a risk factor independent of blood pressure; however, the mechanisms that distinguish pathological remodelling due to local cues from pressure overload are unresolved. This study was aimed at discovering a novel gene expression mechanism in heart failure. In angiotensin II type 1 receptor (AT1R) transgenic mice (TG), we found a significant increase of mRNA and total STAT3 (T-STAT3) protein, but not STAT3 phosphorylated at residues Y705 and S727. A net increase in nuclear accumulation of this unphosphorylated form of STAT3 (U-STAT3) correlated with the development of cardiac hypertrophy and dysfunction, which are associated with abnormal expression of osteopontin and regulator of G protein signalling 2 genes. Nuclear accumulation of U-STAT3 is induced by angiotensin II treatment in neonatal cardiac myocytes, fibroblasts, and AT1R-expressing human embryonic kidney 293 (HEK-AT1R) cells. Chromatin immunoprecipitation demonstrated that U-STAT3 binds to the target gene promoter, and siRNA-mediated knockdown of STAT3 expression significantly altered the expression of target genes in HEK-AT1R cells. T-STAT3 in TG mouse hearts and the phosphorylation-deficient Y705F mutant STAT3 in HEK-AT1R cells physically interacted with transcription co-activator p300. Chronic activation of AT1R induces unregulated expression of the Stat3 gene, leading to nuclear accumulation of U-STAT3, which significantly correlated with progression of cardiac hypertrophy." @default.
• W2022846817 created "2016-06-24" @default.
• W2022846817 creator A5000432967 @default.
• W2022846817 creator A5011980108 @default.
• W2022846817 creator A5070880890 @default.
• W2022846817 creator A5071599807 @default.
• W2022846817 date "2009-08-20" @default.
• W2022846817 modified "2023-10-16" @default.
• W2022846817 title "Role of nuclear unphosphorylated STAT3 in angiotensin II type 1 receptor-induced cardiac hypertrophy" @default.
• W2022846817 cites W1565506774 @default.
• W2022846817 cites W1976140288 @default.
• W2022846817 cites W1978387124 @default.
• W2022846817 cites W1978688282 @default.
• W2022846817 cites W1994479081 @default.
• W2022846817 cites W2008242443 @default.
• W2022846817 cites W2008656746 @default.
• W2022846817 cites W2016134079 @default.
• W2022846817 cites W2017716833 @default.
• W2022846817 cites W2018781549 @default.
• W2022846817 cites W2030865745 @default.
• W2022846817 cites W2031150814 @default.
• W2022846817 cites W2067353642 @default.
• W2022846817 cites W2081557597 @default.
• W2022846817 cites W2085250186 @default.
• W2022846817 cites W2086463427 @default.
• W2022846817 cites W2089919670 @default.
• W2022846817 cites W2103422355 @default.
• W2022846817 cites W2106632219 @default.
• W2022846817 cites W2111704063 @default.
• W2022846817 cites W2116330828 @default.
• W2022846817 cites W2117954320 @default.
• W2022846817 cites W2123746324 @default.
• W2022846817 cites W2129960497 @default.
• W2022846817 cites W2130678592 @default.
• W2022846817 cites W2131666890 @default.
• W2022846817 cites W2135960088 @default.
• W2022846817 cites W2137052264 @default.
• W2022846817 cites W2146487042 @default.
• W2022846817 cites W2151423733 @default.
• W2022846817 cites W2152159778 @default.
• W2022846817 cites W2153496521 @default.
• W2022846817 cites W2154601514 @default.
• W2022846817 cites W2156005120 @default.
• W2022846817 cites W2156835140 @default.
• W2022846817 cites W2161978326 @default.
• W2022846817 cites W4236884809 @default.
• W2022846817 cites W2079379303 @default.
• W2022846817 doi "https://doi.org/10.1093/cvr/cvp285" @default.
• W2022846817 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2791056" @default.
• W2022846817 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19696070" @default.
• W2022846817 hasPublicationYear "2009" @default.
• W2022846817 type Work @default.
• W2022846817 sameAs 2022846817 @default.
• W2022846817 citedByCount "71" @default.
• W2022846817 countsByYear W20228468172012 @default.
• W2022846817 countsByYear W20228468172013 @default.
• W2022846817 countsByYear W20228468172014 @default.
• W2022846817 countsByYear W20228468172015 @default.
• W2022846817 countsByYear W20228468172016 @default.
• W2022846817 countsByYear W20228468172017 @default.
• W2022846817 countsByYear W20228468172018 @default.
• W2022846817 countsByYear W20228468172019 @default.
• W2022846817 countsByYear W20228468172020 @default.
• W2022846817 countsByYear W20228468172021 @default.
• W2022846817 countsByYear W20228468172022 @default.
• W2022846817 countsByYear W20228468172023 @default.
• W2022846817 crossrefType "journal-article" @default.
• W2022846817 hasAuthorship W2022846817A5000432967 @default.
• W2022846817 hasAuthorship W2022846817A5011980108 @default.
• W2022846817 hasAuthorship W2022846817A5070880890 @default.
• W2022846817 hasAuthorship W2022846817A5071599807 @default.
• W2022846817 hasBestOaLocation W20228468171 @default.
• W2022846817 hasConcept C101762097 @default.
• W2022846817 hasConcept C104317684 @default.
• W2022846817 hasConcept C11960822 @default.
• W2022846817 hasConcept C126322002 @default.
• W2022846817 hasConcept C134018914 @default.
• W2022846817 hasConcept C134320426 @default.
• W2022846817 hasConcept C150194340 @default.
• W2022846817 hasConcept C153911025 @default.
• W2022846817 hasConcept C167414201 @default.
• W2022846817 hasConcept C173396325 @default.
• W2022846817 hasConcept C185592680 @default.
• W2022846817 hasConcept C2778271984 @default.
• W2022846817 hasConcept C2778923194 @default.
• W2022846817 hasConcept C2908929049 @default.
• W2022846817 hasConcept C3018791406 @default.
• W2022846817 hasConcept C55493867 @default.
• W2022846817 hasConcept C71924100 @default.
• W2022846817 hasConcept C84393581 @default.
• W2022846817 hasConcept C86339819 @default.
• W2022846817 hasConcept C86803240 @default.
• W2022846817 hasConcept C95444343 @default.
• W2022846817 hasConceptScore W2022846817C101762097 @default.
• W2022846817 hasConceptScore W2022846817C104317684 @default.
• W2022846817 hasConceptScore W2022846817C11960822 @default.
• W2022846817 hasConceptScore W2022846817C126322002 @default.
• W2022846817 hasConceptScore W2022846817C134018914 @default.

• next