FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2014163675> ?p ?o ?g. }

• W2014163675 endingPage "524" @default.
• W2014163675 startingPage "513" @default.
• W2014163675 abstract "BIK (BCL2-interacting killer) is a pro-apoptotic BH3 (BCL2 homology domain 3)-only protein and a member of the BCL2 protein family. It was proposed recently that BIK abundance is controlled by ERK1/2 (extracellular-signal-regulated kinase 1/2)-catalysed phosphorylation, which targets the protein for proteasome-dependent destruction. In the present study, we examined ERK1/2-dependent regulation of BIK, drawing comparisons with BIMEL (BCL2-interacting mediator of cell death; extra long), a well-known target of ERK1/2. In many ERK1/2-dependent tumour cell lines, inhibition of BRAFV600E (v-raf murine sarcoma viral oncogene homologue B1, V600E mutation) or MEK1/2 (mitogen-activated protein kinase/ERK kinase 1/2) had very little effect on BIK expression, whereas BIMEL was strongly up-regulated. In some cell lines we observed a modest increase in BIK expression; however, this was not apparent until ~16 h or later, whereas BIMEL expression increased rapidly within a few hours. Although BIK was degraded by the proteasome, we found no evidence that this was regulated by ERK1/2 signalling. Rather, the delayed increase in BIK expression was prevented by actinomycin D, and was accompanied by increases in BIK mRNA. Finally, the delayed increase in BIK expression following ERK1/2 inhibition was phenocopied by a highly selective CDK4/6 (cyclin-dependent kinases 4 and 6) inhibitor, which caused a strong G1 cell-cycle arrest without inhibiting ERK1/2 signalling. In contrast, BIMEL expression was induced by ERK1/2 inhibition, but not by CDK4/6 inhibition. We conclude that BIK expression is not subject to direct regulation by the ERK1/2 pathway; rather, we propose that BIK expression is cell-cycle-dependent and increases as a consequence of the G1 cell-cycle arrest which results from inhibition of ERK1/2 signalling." @default.
• W2014163675 created "2016-06-24" @default.
• W2014163675 creator A5025815250 @default.
• W2014163675 creator A5080697552 @default.
• W2014163675 date "2014-04-11" @default.
• W2014163675 modified "2023-09-30" @default.
• W2014163675 title "The increase in BIK expression following ERK1/2 pathway inhibition is a consequence of G1 cell-cycle arrest and not a direct effect on BIK protein stability" @default.
• W2014163675 cites W1536449496 @default.
• W2014163675 cites W1816247929 @default.
• W2014163675 cites W1911504906 @default.
• W2014163675 cites W1916509051 @default.
• W2014163675 cites W1963713713 @default.
• W2014163675 cites W1974376685 @default.
• W2014163675 cites W1981256917 @default.
• W2014163675 cites W1990218982 @default.
• W2014163675 cites W1992221435 @default.
• W2014163675 cites W2001558395 @default.
• W2014163675 cites W2005663939 @default.
• W2014163675 cites W2005909927 @default.
• W2014163675 cites W2007687005 @default.
• W2014163675 cites W2008715871 @default.
• W2014163675 cites W2011785467 @default.
• W2014163675 cites W2022096651 @default.
• W2014163675 cites W2032522516 @default.
• W2014163675 cites W2033813420 @default.
• W2014163675 cites W2034057717 @default.
• W2014163675 cites W2036411709 @default.
• W2014163675 cites W2043243100 @default.
• W2014163675 cites W2052788415 @default.
• W2014163675 cites W2058068957 @default.
• W2014163675 cites W2059192510 @default.
• W2014163675 cites W2061727962 @default.
• W2014163675 cites W2064560680 @default.
• W2014163675 cites W2077247436 @default.
• W2014163675 cites W2093628776 @default.
• W2014163675 cites W2094052642 @default.
• W2014163675 cites W2096695840 @default.
• W2014163675 cites W2097007474 @default.
• W2014163675 cites W2097767970 @default.
• W2014163675 cites W2110682589 @default.
• W2014163675 cites W2116787167 @default.
• W2014163675 cites W2117986690 @default.
• W2014163675 cites W2119413773 @default.
• W2014163675 cites W2122549662 @default.
• W2014163675 cites W2136575978 @default.
• W2014163675 cites W2145482514 @default.
• W2014163675 cites W2151971992 @default.
• W2014163675 cites W2167334545 @default.
• W2014163675 cites W2170138574 @default.
• W2014163675 cites W2316080015 @default.
• W2014163675 doi "https://doi.org/10.1042/bj20131346" @default.
• W2014163675 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24527759" @default.
• W2014163675 hasPublicationYear "2014" @default.
• W2014163675 type Work @default.
• W2014163675 sameAs 2014163675 @default.
• W2014163675 citedByCount "4" @default.
• W2014163675 countsByYear W20141636752016 @default.
• W2014163675 countsByYear W20141636752017 @default.
• W2014163675 countsByYear W20141636752019 @default.
• W2014163675 countsByYear W20141636752020 @default.
• W2014163675 crossrefType "journal-article" @default.
• W2014163675 hasAuthorship W2014163675A5025815250 @default.
• W2014163675 hasAuthorship W2014163675A5080697552 @default.
• W2014163675 hasConcept C11960822 @default.
• W2014163675 hasConcept C153911025 @default.
• W2014163675 hasConcept C184235292 @default.
• W2014163675 hasConcept C190283241 @default.
• W2014163675 hasConcept C28406088 @default.
• W2014163675 hasConcept C29537977 @default.
• W2014163675 hasConcept C31573885 @default.
• W2014163675 hasConcept C54355233 @default.
• W2014163675 hasConcept C55493867 @default.
• W2014163675 hasConcept C57074206 @default.
• W2014163675 hasConcept C81885089 @default.
• W2014163675 hasConcept C86803240 @default.
• W2014163675 hasConcept C95444343 @default.
• W2014163675 hasConcept C97029542 @default.
• W2014163675 hasConceptScore W2014163675C11960822 @default.
• W2014163675 hasConceptScore W2014163675C153911025 @default.
• W2014163675 hasConceptScore W2014163675C184235292 @default.
• W2014163675 hasConceptScore W2014163675C190283241 @default.
• W2014163675 hasConceptScore W2014163675C28406088 @default.
• W2014163675 hasConceptScore W2014163675C29537977 @default.
• W2014163675 hasConceptScore W2014163675C31573885 @default.
• W2014163675 hasConceptScore W2014163675C54355233 @default.
• W2014163675 hasConceptScore W2014163675C55493867 @default.
• W2014163675 hasConceptScore W2014163675C57074206 @default.
• W2014163675 hasConceptScore W2014163675C81885089 @default.
• W2014163675 hasConceptScore W2014163675C86803240 @default.
• W2014163675 hasConceptScore W2014163675C95444343 @default.
• W2014163675 hasConceptScore W2014163675C97029542 @default.
• W2014163675 hasIssue "3" @default.
• W2014163675 hasLocation W20141636751 @default.
• W2014163675 hasLocation W20141636752 @default.
• W2014163675 hasOpenAccess W2014163675 @default.
• W2014163675 hasPrimaryLocation W20141636751 @default.
• W2014163675 hasRelatedWork W1518035471 @default.
• W2014163675 hasRelatedWork W1987695408 @default.

• next