FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2108648711> ?p ?o ?g. }

• W2108648711 endingPage "541" @default.
• W2108648711 startingPage "533" @default.
• W2108648711 abstract "Previous studies in hepatocyte-derived cell lines and the whole liver established that the aryl hydrocarbon receptor (AhR) can disrupt G1-phase cell cycle progression following exposure to persistent AhR agonists, such as TCDD (dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin). Growth arrest was attributed to inhibition of G1-phase cyclin-dependent kinase 2 (CDK2) activity. The present study examined the effect of TCDD exposure on liver regeneration following 70% partial hepatectomy in mice lacking the Cip/Kip inhibitors p21(Cip1) or p27(Kip1) responsible for regulating CDK2 activity. Assessment of the regenerative process in wild-type, p21(Cip1) knockout, and p27(Kip1) knockout mice confirmed that TCDD-induced inhibition of liver regeneration is entirely dependent on p21(Cip1) expression. Compared with wild-type mice, the absence of p21(Cip1) expression completely abrogated the TCDD inhibition, and accelerated hepatocyte progression through G1 phase during the regenerative process. Analysis of the transcriptional response determined that increased p21(Cip1) expression during liver regeneration involved an AhR-dependent mechanism. Chromatin immunoprecipitation studies revealed that p21(Cip1) induction required AhR binding to the newly characterized nonconsensus xenobiotic response element, in conjunction with the tumor suppressor protein Kruppel-like factor 6 functioning as an AhR binding partner. The evidence also suggests that AhR functionality following partial hepatectomy is dependent on a p21(Cip1)-regulated signaling process, intimately linking AhR biology to the G1-phase cell cycle program." @default.
• W2108648711 created "2016-06-24" @default.
• W2108648711 creator A5004826404 @default.
• W2108648711 creator A5013757182 @default.
• W2108648711 creator A5022992402 @default.
• W2108648711 creator A5068795845 @default.
• W2108648711 creator A5081421884 @default.
• W2108648711 date "2014-01-15" @default.
• W2108648711 modified "2023-10-02" @default.
• W2108648711 title "Ah Receptor–Mediated Suppression of Liver Regeneration through NC-XRE–Driven p21^Cip1Expression" @default.
• W2108648711 cites W1488712328 @default.
• W2108648711 cites W1530106288 @default.
• W2108648711 cites W1663095249 @default.
• W2108648711 cites W1894737223 @default.
• W2108648711 cites W1935479846 @default.
• W2108648711 cites W1964552446 @default.
• W2108648711 cites W1968601246 @default.
• W2108648711 cites W1971494855 @default.
• W2108648711 cites W1983938442 @default.
• W2108648711 cites W1988290861 @default.
• W2108648711 cites W1989986502 @default.
• W2108648711 cites W1991376447 @default.
• W2108648711 cites W1991592196 @default.
• W2108648711 cites W1996162026 @default.
• W2108648711 cites W1998551192 @default.
• W2108648711 cites W2009225735 @default.
• W2108648711 cites W2015066175 @default.
• W2108648711 cites W2038764863 @default.
• W2108648711 cites W2055795657 @default.
• W2108648711 cites W2064209430 @default.
• W2108648711 cites W2068385015 @default.
• W2108648711 cites W2072088194 @default.
• W2108648711 cites W2072909953 @default.
• W2108648711 cites W2083563797 @default.
• W2108648711 cites W2089069133 @default.
• W2108648711 cites W2097893055 @default.
• W2108648711 cites W2102147956 @default.
• W2108648711 cites W2105900029 @default.
• W2108648711 cites W2108577593 @default.
• W2108648711 cites W2112036584 @default.
• W2108648711 cites W2114629114 @default.
• W2108648711 cites W2118744236 @default.
• W2108648711 cites W2130538892 @default.
• W2108648711 cites W2145337751 @default.
• W2108648711 cites W2146909058 @default.
• W2108648711 cites W2149540498 @default.
• W2108648711 cites W2152107294 @default.
• W2108648711 cites W2152618449 @default.
• W2108648711 cites W2162067613 @default.
• W2108648711 cites W2165627850 @default.
• W2108648711 cites W2165983349 @default.
• W2108648711 cites W2170264506 @default.
• W2108648711 doi "https://doi.org/10.1124/mol.113.089730" @default.
• W2108648711 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3965890" @default.
• W2108648711 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24431146" @default.
• W2108648711 hasPublicationYear "2014" @default.
• W2108648711 type Work @default.
• W2108648711 sameAs 2108648711 @default.
• W2108648711 citedByCount "53" @default.
• W2108648711 countsByYear W21086487112014 @default.
• W2108648711 countsByYear W21086487112015 @default.
• W2108648711 countsByYear W21086487112016 @default.
• W2108648711 countsByYear W21086487112017 @default.
• W2108648711 countsByYear W21086487112018 @default.
• W2108648711 countsByYear W21086487112019 @default.
• W2108648711 countsByYear W21086487112020 @default.
• W2108648711 countsByYear W21086487112021 @default.
• W2108648711 countsByYear W21086487112022 @default.
• W2108648711 countsByYear W21086487112023 @default.
• W2108648711 crossrefType "journal-article" @default.
• W2108648711 hasAuthorship W2108648711A5004826404 @default.
• W2108648711 hasAuthorship W2108648711A5013757182 @default.
• W2108648711 hasAuthorship W2108648711A5022992402 @default.
• W2108648711 hasAuthorship W2108648711A5068795845 @default.
• W2108648711 hasAuthorship W2108648711A5081421884 @default.
• W2108648711 hasBestOaLocation W21086487112 @default.
• W2108648711 hasConcept C101762097 @default.
• W2108648711 hasConcept C104317684 @default.
• W2108648711 hasConcept C124320809 @default.
• W2108648711 hasConcept C126322002 @default.
• W2108648711 hasConcept C134018914 @default.
• W2108648711 hasConcept C134320426 @default.
• W2108648711 hasConcept C1491633281 @default.
• W2108648711 hasConcept C150194340 @default.
• W2108648711 hasConcept C153911025 @default.
• W2108648711 hasConcept C171056886 @default.
• W2108648711 hasConcept C184235292 @default.
• W2108648711 hasConcept C185592680 @default.
• W2108648711 hasConcept C202751555 @default.
• W2108648711 hasConcept C2776200302 @default.
• W2108648711 hasConcept C2776795407 @default.
• W2108648711 hasConcept C29537977 @default.
• W2108648711 hasConcept C33594762 @default.
• W2108648711 hasConcept C55493867 @default.
• W2108648711 hasConcept C62112901 @default.
• W2108648711 hasConcept C71924100 @default.
• W2108648711 hasConcept C82495950 @default.
• W2108648711 hasConcept C86339819 @default.

• next