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dc.contributor.authorKatzav, Shulamit
dc.contributor.authorSchmitz, M. Lienhard
dc.date.accessioned2022-11-18T09:51:02Z
dc.date.available2016-02-25T14:07:43Z
dc.date.available2022-11-18T09:51:02Z
dc.date.issued2015
dc.identifier.urihttp://nbn-resolving.de/urn:nbn:de:hebis:26-opus-119749
dc.identifier.urihttps://jlupub.ub.uni-giessen.de//handle/jlupub/9177
dc.identifier.urihttp://dx.doi.org/10.22029/jlupub-8565
dc.description.abstractNext generation sequencing has shown the frequent occurrence of point mutations in the ubiquitin E3 ligase c-Cbl in myeloid malignancies. Mouse models revealed a causal contribution of c-Cbl for the onset of such neoplasms. The point mutations typically cluster in the linker region and RING finger domain and affect both alleles by acquired uniparental disomy. The fast progress in the detection of c-Cbl mutations is contrasted by our scarce knowledge on their functional consequences. The c-Cbl protein displays several enzymatic functions by promoting the attachment of differentially composed ubiquitin chains and of the ubiquitin-like protein NEDD8 to its target proteins. In addition, c-Cbl functions as an adapter protein and undergoes phosphorylation-dependent inducible conformation changes. Studies on the impact of c-Cbl mutations on its functions as a dynamic and versatile adapter protein, its interactomes and on its various enzymatic activities are now important to allow the identification of druggable targets within the c-Cbl signaling network.en
dc.language.isoende_DE
dc.rightsNamensnennung 3.0 International*
dc.rights.urihttps://creativecommons.org/licenses/by/3.0/*
dc.subjectcblen
dc.subjectmyeloid malignanciesen
dc.subject.ddcddc:610de_DE
dc.titleMutations of c-Cbl in myeloid malignanciesen
dc.typearticlede_DE
local.affiliationFB 11 - Medizinde_DE
local.opus.id11974
local.opus.instituteInstitute of Biochemistryde_DE
local.opus.fachgebietMedizinde_DE
local.source.urihttps://doi.org/
local.source.freetextOncotarget 6(13):10689-10696de_DE


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