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dc.contributor.authorKumar, Sushilen_US
dc.contributor.authorLu, Binen_US
dc.contributor.authorDixit, Updeshen_US
dc.contributor.authorHossain, Sajjaden_US
dc.contributor.authorLiu, Yongzhangen_US
dc.contributor.authorLi, Jingen_US
dc.contributor.authorHornbeck, Peteren_US
dc.contributor.authorZheng, Weimingen_US
dc.contributor.authorSowalsky, Adam G.en_US
dc.contributor.authorKotula, Leszeken_US
dc.contributor.authorBirge, Raymond B.en_US
dc.date.accessioned2016-04-01T15:48:17Z
dc.date.issued2015en_US
dc.identifier.citationKumar, S., B. Lu, U. Dixit, S. Hossain, Y. Liu, J. Li, P. Hornbeck, et al. 2015. “Reciprocal regulation of Abl kinase by Crk Y251 and Abi1 controls invasive phenotypes in glioblastoma.” Oncotarget 6 (35): 37792-37807.en
dc.identifier.issn1949-2553en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:26318678
dc.description.abstractCrk is the prototypical member of a class of Src homology 2 (SH2) and Src homology 3 (SH3) domain-containing adaptor proteins that positively regulate cell motility via the activation of Rac1 and, in certain tumor types such as GBM, can promote cell invasion and metastasis by mechanisms that are not well understood. Here we demonstrate that Crk, via its phosphorylation at Tyr251, promotes invasive behavior of tumor cells, is a prominent feature in GBM, and correlating with aggressive glioma grade IV staging and overall poor survival outcomes. At the molecular level, Tyr251 phosphorylation of Crk is negatively regulated by Abi1, which competes for Crk binding to Abl and attenuates Abl transactivation. Together, these results show that Crk and Abi1 have reciprocal biological effects and act as a molecular rheostat to control Abl activation and cell invasion. Finally, these data suggest that Crk Tyr251 phosphorylation regulate invasive cell phenotypes and may serve as a biomarker for aggressive GBM.en
dc.language.isoen_USen
dc.publisherImpact Journals LLCen
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4741966/pdf/en
dash.licenseLAAen_US
dc.subjectnon-canonical Crk signalingen
dc.subjectAbi1en
dc.subjectglioblastoma multiformaeen
dc.subjectcell invasionen
dc.titleReciprocal regulation of Abl kinase by Crk Y251 and Abi1 controls invasive phenotypes in glioblastomaen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalOncotargeten
dc.date.available2016-04-01T15:48:17Z
dash.authorsorderedfalse


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