FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2045975035> ?p ?o ?g. }

• W2045975035 endingPage "6003" @default.
• W2045975035 startingPage "5997" @default.
• W2045975035 abstract "Many solid tumors contain substantial fractions of hypoxic cells which are relatively resistant to both radiation therapy and certain cytotoxic drugs. We have previously shown that exposure of human HT29 cells to hypoxic conditions results in the overexpression of certain enzymes involved in the detoxication of xenobiotics, including NAD(P)H:(quinone acceptor) oxidoreductase (DT)-diaphorase, and gamma-glutamylcysteine synthetase, the rate-limiting enzyme in glutathione synthesis. This hypoxic effect on DT-diaphorase was shown to involve both transcriptional induction and altered message stability. We have investigated the effects of hypoxia on elements in the promoter region of DT-diaphorase. Electrophoretic mobility shift assays demonstrate the induction of a binding activity to the AP-1 response element of DT-diaphorase. Supershift assays suggest that this binding is due to AP-1 nuclear factors and that members of the jun family are induced to a greater degree than fos by hypoxia. Analysis of the kinetics of transcription factor expression indicates that the expression of c-jun and junD is induced during hypoxic exposure; mRNA levels fall during reoxygenation. Induction of fos on the other hand is not as florid during hypoxia (5-fold) and is most pronounced (17-fold) 24 h after the restoration of an oxic environment. Thus, the hypoxic response of DT-diaphorase expression is mediated in part through AP-1, initially by a jun-related mechanism and then by the involvement of fos. The affinity of transcription factors for the AP-1 binding site depends on the redox state of a cysteine residue located close to the DNA-binding region of both Fos and Jun. A nuclear protein, Ref-1, maintains the reduced state of Fos and Jun and promotes binding to AP-1. Nuclear extracts of HT29 cells exposed to hypoxia show markedly increased Ref-1 protein content. Elevation of ref-1 steady-state mRNA levels occurs as an early event following induction of hypoxia and persists when cells are restored to a normally oxygenated environment. Nuclear run-on analysis demonstrates that induction of transcription is the mechanism of ref-1 mRNA elevation. Electrophoretic mobility shift assays and immunodepletion assays were used to further define the interaction of Ref-1 with specific AP-1-binding proteins under hypoxic conditions. These data demonstrate that the induction of detoxicating enzyme expression in HT29 cells exposed to hypoxia results from the induction of both transactivating factors that bind to the AP-1 element and of redox proteins that enhance their affinity for this element." @default.
• W2045975035 created "2016-06-24" @default.
• W2045975035 creator A5006841058 @default.
• W2045975035 creator A5028533192 @default.
• W2045975035 creator A5048595906 @default.
• W2045975035 creator A5068821884 @default.
• W2045975035 date "1994-09-01" @default.
• W2045975035 modified "2023-10-16" @default.
• W2045975035 title "Activation of AP-1 and of a nuclear redox factor, Ref-1, in the response of HT29 colon cancer cells to hypoxia." @default.
• W2045975035 cites W1483046275 @default.
• W2045975035 cites W1501434619 @default.
• W2045975035 cites W1503662436 @default.
• W2045975035 cites W1530430636 @default.
• W2045975035 cites W1542431794 @default.
• W2045975035 cites W1601634511 @default.
• W2045975035 cites W1603378617 @default.
• W2045975035 cites W1604748982 @default.
• W2045975035 cites W167451947 @default.
• W2045975035 cites W1815879748 @default.
• W2045975035 cites W1833314013 @default.
• W2045975035 cites W1833690096 @default.
• W2045975035 cites W1849269729 @default.
• W2045975035 cites W1861749169 @default.
• W2045975035 cites W1903192662 @default.
• W2045975035 cites W1932728046 @default.
• W2045975035 cites W1949973946 @default.
• W2045975035 cites W1964306615 @default.
• W2045975035 cites W1972241251 @default.
• W2045975035 cites W1972323173 @default.
• W2045975035 cites W1972626671 @default.
• W2045975035 cites W1974750292 @default.
• W2045975035 cites W1978659501 @default.
• W2045975035 cites W1993243592 @default.
• W2045975035 cites W2001945975 @default.
• W2045975035 cites W2013436421 @default.
• W2045975035 cites W2020165283 @default.
• W2045975035 cites W2042917826 @default.
• W2045975035 cites W2049088667 @default.
• W2045975035 cites W2057094603 @default.
• W2045975035 cites W2070693959 @default.
• W2045975035 cites W2073218573 @default.
• W2045975035 cites W2082125920 @default.
• W2045975035 cites W2085016751 @default.
• W2045975035 cites W2101108802 @default.
• W2045975035 cites W2101521188 @default.
• W2045975035 cites W2134812217 @default.
• W2045975035 cites W2139338030 @default.
• W2045975035 cites W2141639935 @default.
• W2045975035 cites W2149175606 @default.
• W2045975035 cites W2167229055 @default.
• W2045975035 cites W2231666798 @default.
• W2045975035 cites W2413463688 @default.
• W2045975035 cites W2417705998 @default.
• W2045975035 cites W2418295025 @default.
• W2045975035 doi "https://doi.org/10.1128/mcb.14.9.5997" @default.
• W2045975035 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/359125" @default.
• W2045975035 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8065332" @default.
• W2045975035 hasPublicationYear "1994" @default.
• W2045975035 type Work @default.
• W2045975035 sameAs 2045975035 @default.
• W2045975035 citedByCount "207" @default.
• W2045975035 countsByYear W20459750352012 @default.
• W2045975035 countsByYear W20459750352013 @default.
• W2045975035 countsByYear W20459750352014 @default.
• W2045975035 countsByYear W20459750352015 @default.
• W2045975035 countsByYear W20459750352016 @default.
• W2045975035 countsByYear W20459750352017 @default.
• W2045975035 crossrefType "journal-article" @default.
• W2045975035 hasAuthorship W2045975035A5006841058 @default.
• W2045975035 hasAuthorship W2045975035A5028533192 @default.
• W2045975035 hasAuthorship W2045975035A5048595906 @default.
• W2045975035 hasAuthorship W2045975035A5068821884 @default.
• W2045975035 hasBestOaLocation W20459750351 @default.
• W2045975035 hasConcept C104317684 @default.
• W2045975035 hasConcept C107824862 @default.
• W2045975035 hasConcept C138885662 @default.
• W2045975035 hasConcept C153911025 @default.
• W2045975035 hasConcept C178790620 @default.
• W2045975035 hasConcept C179926584 @default.
• W2045975035 hasConcept C181199279 @default.
• W2045975035 hasConcept C183978625 @default.
• W2045975035 hasConcept C185592680 @default.
• W2045975035 hasConcept C2779201268 @default.
• W2045975035 hasConcept C41895202 @default.
• W2045975035 hasConcept C538909803 @default.
• W2045975035 hasConcept C540031477 @default.
• W2045975035 hasConcept C55493867 @default.
• W2045975035 hasConcept C75520062 @default.
• W2045975035 hasConcept C7836513 @default.
• W2045975035 hasConcept C86339819 @default.
• W2045975035 hasConcept C86803240 @default.
• W2045975035 hasConceptScore W2045975035C104317684 @default.
• W2045975035 hasConceptScore W2045975035C107824862 @default.
• W2045975035 hasConceptScore W2045975035C138885662 @default.
• W2045975035 hasConceptScore W2045975035C153911025 @default.
• W2045975035 hasConceptScore W2045975035C178790620 @default.
• W2045975035 hasConceptScore W2045975035C179926584 @default.
• W2045975035 hasConceptScore W2045975035C181199279 @default.

• next