FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2061067369> ?p ?o ?g. }

• W2061067369 endingPage "e1535" @default.
• W2061067369 startingPage "e1535" @default.
• W2061067369 abstract "Abstract P27 was identified as a tumor suppressor nearly two decades, being implicated in cell-cycle control, differentiation, senescence, apoptosis and motility. Our present study, for the first time to the best of our knowledge, revealed a potential role of p27 in inhibiting S6-mediated hypoxia-inducible factor-1 α (HIF-1 α ) protein translation, which contributed to the protection from environmental carcinogen (sodium arsenite)-induced cell transformation. Our findings showed that depletion of p27 expression by knockout and knockdown approaches efficiently enhanced S6 phosphorylation in arsenite response via overactivating Ras/Raf/MEK/ERK pathway, which consequently resulted in the stimulation of p90RSK (90 kDa ribosomal S6 kinase), a direct kinase for S6 phosphorylation. Although PI3K/AKT pathway was also involved in S6 activation, blocking AKT and p70S6K activation did not attenuate arsenite-induced S6 activation in p27−/− cells, suggesting p27 specifically targeted Ras/ERK pathway rather than PI3K/AKT pathway for inhibition of S6 activation in response to arsenite exposure. Further functional studies found that p27 had a negative role in cell transformation induced by chronic low-dose arsentie exposure. Mechanistic investigations showed that HIF-1 α translation was upregulated in p27-deficient cells in an S6 phosphorylation-dependent manner and functioned as a driving force in arsenite-induced cell transformation. Knockdown of HIF-1 α efficiently reversed arsenite-induced cell transformation in p27-depleted cells. Taken together, our findings provided strong evidence showing that by targeting Ras/ERK pathway, p27 provided a negative control over HIF-1 α protein synthesis in an S6-dependent manner, and abrogated arsenite-induced cell transformation via downregulation of HIF-1 α translation." @default.
• W2061067369 created "2016-06-24" @default.
• W2061067369 creator A5005133589 @default.
• W2061067369 creator A5018153471 @default.
• W2061067369 creator A5025524154 @default.
• W2061067369 creator A5052119066 @default.
• W2061067369 creator A5057100969 @default.
• W2061067369 creator A5062247956 @default.
• W2061067369 date "2014-11-20" @default.
• W2061067369 modified "2023-10-16" @default.
• W2061067369 title "The N-terminal region of p27 inhibits HIF-1α protein translation in ribosomal protein S6-dependent manner by regulating PHLPP-Ras-ERK-p90RSK axis" @default.
• W2061067369 cites W1523062737 @default.
• W2061067369 cites W153199275 @default.
• W2061067369 cites W1563594465 @default.
• W2061067369 cites W1579876257 @default.
• W2061067369 cites W1634346462 @default.
• W2061067369 cites W173536926 @default.
• W2061067369 cites W1964115507 @default.
• W2061067369 cites W1964201687 @default.
• W2061067369 cites W1966995656 @default.
• W2061067369 cites W1974574293 @default.
• W2061067369 cites W1978345311 @default.
• W2061067369 cites W1978746682 @default.
• W2061067369 cites W1983958620 @default.
• W2061067369 cites W1987009453 @default.
• W2061067369 cites W1995561104 @default.
• W2061067369 cites W1995681499 @default.
• W2061067369 cites W2000969116 @default.
• W2061067369 cites W2001220887 @default.
• W2061067369 cites W2018782901 @default.
• W2061067369 cites W2019716859 @default.
• W2061067369 cites W2022117140 @default.
• W2061067369 cites W2026004604 @default.
• W2061067369 cites W2027690266 @default.
• W2061067369 cites W2030986659 @default.
• W2061067369 cites W2031325927 @default.
• W2061067369 cites W2038137623 @default.
• W2061067369 cites W2039916144 @default.
• W2061067369 cites W2042598897 @default.
• W2061067369 cites W2045296432 @default.
• W2061067369 cites W2049283940 @default.
• W2061067369 cites W2049834195 @default.
• W2061067369 cites W2052060197 @default.
• W2061067369 cites W2055072807 @default.
• W2061067369 cites W2056806077 @default.
• W2061067369 cites W2058588605 @default.
• W2061067369 cites W2061988426 @default.
• W2061067369 cites W2066700256 @default.
• W2061067369 cites W2070660235 @default.
• W2061067369 cites W2071394735 @default.
• W2061067369 cites W2074503707 @default.
• W2061067369 cites W2077456443 @default.
• W2061067369 cites W2078275626 @default.
• W2061067369 cites W2083561654 @default.
• W2061067369 cites W2090975426 @default.
• W2061067369 cites W2091729097 @default.
• W2061067369 cites W2103732635 @default.
• W2061067369 cites W2107744784 @default.
• W2061067369 cites W2116711648 @default.
• W2061067369 cites W2118750047 @default.
• W2061067369 cites W2130811967 @default.
• W2061067369 cites W2140899494 @default.
• W2061067369 cites W2156363172 @default.
• W2061067369 cites W2157754963 @default.
• W2061067369 cites W2157831802 @default.
• W2061067369 cites W2161135924 @default.
• W2061067369 cites W2161451268 @default.
• W2061067369 cites W2284952923 @default.
• W2061067369 cites W2319395364 @default.
• W2061067369 doi "https://doi.org/10.1038/cddis.2014.496" @default.
• W2061067369 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4260754" @default.
• W2061067369 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25412313" @default.
• W2061067369 hasPublicationYear "2014" @default.
• W2061067369 type Work @default.
• W2061067369 sameAs 2061067369 @default.
• W2061067369 citedByCount "17" @default.
• W2061067369 countsByYear W20610673692016 @default.
• W2061067369 countsByYear W20610673692017 @default.
• W2061067369 countsByYear W20610673692018 @default.
• W2061067369 countsByYear W20610673692019 @default.
• W2061067369 countsByYear W20610673692020 @default.
• W2061067369 countsByYear W20610673692021 @default.
• W2061067369 countsByYear W20610673692022 @default.
• W2061067369 countsByYear W20610673692023 @default.
• W2061067369 crossrefType "journal-article" @default.
• W2061067369 hasAuthorship W2061067369A5005133589 @default.
• W2061067369 hasAuthorship W2061067369A5018153471 @default.
• W2061067369 hasAuthorship W2061067369A5025524154 @default.
• W2061067369 hasAuthorship W2061067369A5052119066 @default.
• W2061067369 hasAuthorship W2061067369A5057100969 @default.
• W2061067369 hasAuthorship W2061067369A5062247956 @default.
• W2061067369 hasBestOaLocation W20610673691 @default.
• W2061067369 hasConcept C104202773 @default.
• W2061067369 hasConcept C11960822 @default.
• W2061067369 hasConcept C178790620 @default.
• W2061067369 hasConcept C184235292 @default.
• W2061067369 hasConcept C185592680 @default.
• W2061067369 hasConcept C2776305511 @default.

• next