FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3122290422> ?p ?o ?g. }

• W3122290422 endingPage "166080" @default.
• W3122290422 startingPage "166080" @default.
• W3122290422 abstract "The peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α) regulates metabolism and is essential for normal cardiac function. Its activity is suppressed during pressure overload induced cardiac hypertrophy and such suppression at least partially contributes to the associated morbidity. The O-linked β- N -acetylglucosamine post-translational modification (O-GlcNAc) of proteins is a glucose-derived metabolic signal. The relationship between O-GlcNAc, and PGC-1α activity in cardiac hypertrophy is unknown. We hypothesized that hypertrophy-induced suppression of PGC-1α was at least partially regulated by O-GlcNAc signaling. Treatment of neonatal rat cardiac myocytes with phenylephrine (an inducer of cardiomyocyte hypertrophy) significantly enhanced global O-GlcNAc signaling. Quantitative real-time PCR analysis revealed a downregulation of PGC-1α with concomitant suppression of fatty acid oxidation/mitochondrial genes. Transverse aortic constriction in mice decreased the basal expression of PGC-1α and its downstream genes. Reduction of O-GlcNAc signaling alleviated suppression of PGC-1α and most of its downstream genes. Interestingly, augmentation of O-GlcNAc signaling with glucosamine or PUGNAC (a O-GlcNAcase inhibitor) reduced glucose starvation-induced PGC-1α upregulation even in the absence of hypertrophy. Finally, we found that PGC-1α itself is O-GlcNAcylated. Together, these results reveal the recruitment of O-GlcNAc signaling as a potentially novel regulator of PGC-1α activity during cardiac hypertrophy. Furthermore, O-GlcNAc signaling may mediate constitutive suppression of PGC-1α activity in the heart. Such findings illuminate new possibilities regarding the inter-regulation of O-GlcNAc signaling and also may have some implications for metabolic dysregulation during cardiac diseases. • Cardiac hypertrophy enhances protein O-glycosylation. • O-GlcNAc signaling modifies PGC-1a. • O-glycosylation of proteins supress PGC-1a levels and transcripts. • Blocking O-GlcNAc signaling reverses PGC-1a repression during in vitro cardiac hypertrophy." @default.
• W3122290422 created "2021-02-01" @default.
• W3122290422 creator A5036904418 @default.
• W3122290422 creator A5075931216 @default.
• W3122290422 date "2021-05-01" @default.
• W3122290422 modified "2023-10-02" @default.
• W3122290422 title "Cardiac hypertrophy drives PGC-1α suppression associated with enhanced O-glycosylation" @default.
• W3122290422 cites W1896434730 @default.
• W3122290422 cites W1970261233 @default.
• W3122290422 cites W1971082641 @default.
• W3122290422 cites W1975346170 @default.
• W3122290422 cites W1975959667 @default.
• W3122290422 cites W1993790829 @default.
• W3122290422 cites W2002888609 @default.
• W3122290422 cites W2011182719 @default.
• W3122290422 cites W2016015885 @default.
• W3122290422 cites W2017741706 @default.
• W3122290422 cites W2025577759 @default.
• W3122290422 cites W2047754708 @default.
• W3122290422 cites W2048874320 @default.
• W3122290422 cites W2060973911 @default.
• W3122290422 cites W2074332237 @default.
• W3122290422 cites W2078075091 @default.
• W3122290422 cites W2081098379 @default.
• W3122290422 cites W2082984525 @default.
• W3122290422 cites W2094005996 @default.
• W3122290422 cites W2094420876 @default.
• W3122290422 cites W2103634232 @default.
• W3122290422 cites W2105404724 @default.
• W3122290422 cites W2113181569 @default.
• W3122290422 cites W2113515610 @default.
• W3122290422 cites W2138718614 @default.
• W3122290422 cites W2150191367 @default.
• W3122290422 cites W2152205887 @default.
• W3122290422 cites W2160909177 @default.
• W3122290422 cites W2342386520 @default.
• W3122290422 cites W2394826799 @default.
• W3122290422 cites W2605795476 @default.
• W3122290422 cites W2890285951 @default.
• W3122290422 cites W2908792424 @default.
• W3122290422 cites W2911143204 @default.
• W3122290422 cites W3003674302 @default.
• W3122290422 doi "https://doi.org/10.1016/j.bbadis.2021.166080" @default.
• W3122290422 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33486096" @default.
• W3122290422 hasPublicationYear "2021" @default.
• W3122290422 type Work @default.
• W3122290422 sameAs 3122290422 @default.
• W3122290422 citedByCount "10" @default.
• W3122290422 countsByYear W31222904222021 @default.
• W3122290422 countsByYear W31222904222022 @default.
• W3122290422 countsByYear W31222904222023 @default.
• W3122290422 crossrefType "journal-article" @default.
• W3122290422 hasAuthorship W3122290422A5036904418 @default.
• W3122290422 hasAuthorship W3122290422A5075931216 @default.
• W3122290422 hasBestOaLocation W31222904221 @default.
• W3122290422 hasConcept C126322002 @default.
• W3122290422 hasConcept C134018914 @default.
• W3122290422 hasConcept C164705383 @default.
• W3122290422 hasConcept C167414201 @default.
• W3122290422 hasConcept C185592680 @default.
• W3122290422 hasConcept C2777313579 @default.
• W3122290422 hasConcept C3018791406 @default.
• W3122290422 hasConcept C55493867 @default.
• W3122290422 hasConcept C71924100 @default.
• W3122290422 hasConcept C86803240 @default.
• W3122290422 hasConcept C95444343 @default.
• W3122290422 hasConceptScore W3122290422C126322002 @default.
• W3122290422 hasConceptScore W3122290422C134018914 @default.
• W3122290422 hasConceptScore W3122290422C164705383 @default.
• W3122290422 hasConceptScore W3122290422C167414201 @default.
• W3122290422 hasConceptScore W3122290422C185592680 @default.
• W3122290422 hasConceptScore W3122290422C2777313579 @default.
• W3122290422 hasConceptScore W3122290422C3018791406 @default.
• W3122290422 hasConceptScore W3122290422C55493867 @default.
• W3122290422 hasConceptScore W3122290422C71924100 @default.
• W3122290422 hasConceptScore W3122290422C86803240 @default.
• W3122290422 hasConceptScore W3122290422C95444343 @default.
• W3122290422 hasFunder F4320306230 @default.
• W3122290422 hasIssue "5" @default.
• W3122290422 hasLocation W31222904221 @default.
• W3122290422 hasOpenAccess W3122290422 @default.
• W3122290422 hasPrimaryLocation W31222904221 @default.
• W3122290422 hasRelatedWork W1514902666 @default.
• W3122290422 hasRelatedWork W1779480512 @default.
• W3122290422 hasRelatedWork W1981654342 @default.
• W3122290422 hasRelatedWork W1993394218 @default.
• W3122290422 hasRelatedWork W1993774701 @default.
• W3122290422 hasRelatedWork W2021603989 @default.
• W3122290422 hasRelatedWork W2081636567 @default.
• W3122290422 hasRelatedWork W2091504832 @default.
• W3122290422 hasRelatedWork W2111395426 @default.
• W3122290422 hasRelatedWork W2748952813 @default.
• W3122290422 hasVolume "1867" @default.
• W3122290422 isParatext "false" @default.
• W3122290422 isRetracted "false" @default.
• W3122290422 magId "3122290422" @default.
• W3122290422 workType "article" @default.