Matches in SemOpenAlex for { <https://semopenalex.org/work/W2892630669> ?p ?o ?g. }
- W2892630669 endingPage "e1007697" @default.
- W2892630669 startingPage "e1007697" @default.
- W2892630669 abstract "Lgr5+ intestinal stem cells are crucial for fast homeostatic renewal of intestinal epithelium and Wnt/β-catenin signaling plays an essential role in this process by sustaining stem cell self-renewal. The poly(ADP-ribose) polymerases tankyrases (TNKSs) mediate protein poly-ADP-ribosylation and are involved in multiple cellular processes such as Wnt signaling regulation, mitotic progression and telomere maintenance. However, little is known about the physiological function of TNKSs in epithelium homeostasis regulation. Here, using Villin-creERT2;Tnks1-/-;Tnks2fl/fl (DKO) mice, we observed that loss of TNKSs causes a rapid decrease of Lgr5+ intestinal stem cells and magnified apoptosis in small intestinal crypts, leading to intestine degeneration and increased mouse mortality. Consistently, deletion of Tnks or blockage of TNKS activity with the inhibitor XAV939 significantly inhibits the growth of intestinal organoids. We further showed that the Wnt signaling agonist CHIR99021 sustains the growth of DKO organoids, and XAV939 does not cause growth retardation of Apc-/- organoids. Consistent with the promoting function of TNKSs in Wnt signaling, Wnt/β-catenin signaling is significantly decreased with stabilized Axin in DKO crypts. Together, our findings unravel the essential role of TNKSs-mediated protein parsylation in small intestinal homeostasis by modulating Wnt/β-catenin signaling." @default.
- W2892630669 created "2018-10-05" @default.
- W2892630669 creator A5012949593 @default.
- W2892630669 creator A5025012207 @default.
- W2892630669 creator A5025824933 @default.
- W2892630669 creator A5031295186 @default.
- W2892630669 creator A5044622075 @default.
- W2892630669 creator A5046214153 @default.
- W2892630669 creator A5075333074 @default.
- W2892630669 creator A5081866945 @default.
- W2892630669 date "2018-09-27" @default.
- W2892630669 modified "2023-10-17" @default.
- W2892630669 title "Tankyrases maintain homeostasis of intestinal epithelium by preventing cell death" @default.
- W2892630669 cites W1939041072 @default.
- W2892630669 cites W1965006127 @default.
- W2892630669 cites W1979313505 @default.
- W2892630669 cites W1982603620 @default.
- W2892630669 cites W1993748871 @default.
- W2892630669 cites W1996583924 @default.
- W2892630669 cites W2006419043 @default.
- W2892630669 cites W2008557163 @default.
- W2892630669 cites W2008952211 @default.
- W2892630669 cites W2009295603 @default.
- W2892630669 cites W2012565727 @default.
- W2892630669 cites W2016020712 @default.
- W2892630669 cites W2017218715 @default.
- W2892630669 cites W2023906737 @default.
- W2892630669 cites W2030777235 @default.
- W2892630669 cites W2039031756 @default.
- W2892630669 cites W2040731170 @default.
- W2892630669 cites W2051294804 @default.
- W2892630669 cites W2053352622 @default.
- W2892630669 cites W2057257265 @default.
- W2892630669 cites W2065585161 @default.
- W2892630669 cites W2065878510 @default.
- W2892630669 cites W2078651829 @default.
- W2892630669 cites W2088689845 @default.
- W2892630669 cites W2092672926 @default.
- W2892630669 cites W2094343813 @default.
- W2892630669 cites W2098201429 @default.
- W2892630669 cites W2101889783 @default.
- W2892630669 cites W2104297850 @default.
- W2892630669 cites W2105240743 @default.
- W2892630669 cites W2110321854 @default.
- W2892630669 cites W2112671059 @default.
- W2892630669 cites W2123639013 @default.
- W2892630669 cites W2127251209 @default.
- W2892630669 cites W2134137083 @default.
- W2892630669 cites W2141185701 @default.
- W2892630669 cites W2143625921 @default.
- W2892630669 cites W2144311146 @default.
- W2892630669 cites W2145955680 @default.
- W2892630669 cites W2151436498 @default.
- W2892630669 cites W2155170442 @default.
- W2892630669 cites W2157010562 @default.
- W2892630669 cites W2158021558 @default.
- W2892630669 cites W2159155233 @default.
- W2892630669 cites W2165720306 @default.
- W2892630669 cites W2171125452 @default.
- W2892630669 cites W2209116386 @default.
- W2892630669 cites W2252829562 @default.
- W2892630669 cites W2260331015 @default.
- W2892630669 cites W2400176516 @default.
- W2892630669 cites W2567946031 @default.
- W2892630669 cites W2611779918 @default.
- W2892630669 cites W2621361823 @default.
- W2892630669 cites W2624004946 @default.
- W2892630669 cites W2752378015 @default.
- W2892630669 cites W2765414974 @default.
- W2892630669 cites W2767300971 @default.
- W2892630669 cites W2767684755 @default.
- W2892630669 cites W98434679 @default.
- W2892630669 doi "https://doi.org/10.1371/journal.pgen.1007697" @default.
- W2892630669 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6177203" @default.
- W2892630669 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30260955" @default.
- W2892630669 hasPublicationYear "2018" @default.
- W2892630669 type Work @default.
- W2892630669 sameAs 2892630669 @default.
- W2892630669 citedByCount "9" @default.
- W2892630669 countsByYear W28926306692019 @default.
- W2892630669 countsByYear W28926306692020 @default.
- W2892630669 countsByYear W28926306692021 @default.
- W2892630669 countsByYear W28926306692022 @default.
- W2892630669 countsByYear W28926306692023 @default.
- W2892630669 crossrefType "journal-article" @default.
- W2892630669 hasAuthorship W2892630669A5012949593 @default.
- W2892630669 hasAuthorship W2892630669A5025012207 @default.
- W2892630669 hasAuthorship W2892630669A5025824933 @default.
- W2892630669 hasAuthorship W2892630669A5031295186 @default.
- W2892630669 hasAuthorship W2892630669A5044622075 @default.
- W2892630669 hasAuthorship W2892630669A5046214153 @default.
- W2892630669 hasAuthorship W2892630669A5075333074 @default.
- W2892630669 hasAuthorship W2892630669A5081866945 @default.
- W2892630669 hasBestOaLocation W28926306691 @default.
- W2892630669 hasConcept C10116572 @default.
- W2892630669 hasConcept C126322002 @default.
- W2892630669 hasConcept C134018914 @default.
- W2892630669 hasConcept C137620995 @default.