Mostrar el registro sencillo del ítem

dc.contributor.authorLim, R
dc.contributor.authorSugino, T
dc.contributor.authorNolte, H
dc.contributor.authorAndrade, J
dc.contributor.authorZimmermann, B
dc.contributor.authorShi, C
dc.contributor.authorDoddaballapur, A
dc.contributor.authorOng, Y T
dc.contributor.authorWilhelm, K
dc.contributor.authorFasse, J W D
dc.contributor.authorErnst, A
dc.contributor.authorKaulich, M
dc.contributor.authorHusnjak, K
dc.contributor.authorBoettger, T
dc.contributor.authorGuenther, S
dc.contributor.authorBraun, T
dc.contributor.authorKrüger, M
dc.contributor.authorBenedito, Rui 
dc.contributor.authorDikic, I
dc.contributor.authorPotente, M
dc.date.accessioned2020-04-22T16:00:30Z
dc.date.available2020-04-22T16:00:30Z
dc.date.issued2019-04
dc.identifier.citationScience. 2019; 364(6436):188-193es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/9685
dc.description.abstractNotch signaling is a core patterning module for vascular morphogenesis that codetermines the sprouting behavior of endothelial cells (ECs). Tight quantitative and temporal control of Notch activity is essential for vascular development, yet the details of Notch regulation in ECs are incompletely understood. We found that ubiquitin-specific peptidase 10 (USP10) interacted with the NOTCH1 intracellular domain (NICD1) to slow the ubiquitin-dependent turnover of this short-lived form of the activated NOTCH1 receptor. Accordingly, inactivation of USP10 reduced NICD1 abundance and stability and diminished Notch-induced target gene expression in ECs. In mice, the loss of endothelial Usp10 increased vessel sprouting and partially restored the patterning defects caused by ectopic expression of NICD1. Thus, USP10 functions as an NICD1 deubiquitinase that fine-tunes endothelial Notch responses during angiogenic sprouting.es_ES
dc.description.sponsorshipThis work is supported by the Max Planck Society, European Research Council (ERC) starting grant ANGIOMET (311546), ERC consolidator grant EMERGE (773047), the Deutsche Forschungsgemeinschaft (SFB 834), the Excellence Cluster Cardiopulmonary System (EXC 147/1), LOEWE grant Ub-Net, the DZHK (German Center for Cardiovascular Research), the Stiftung Charité, the Cardio-Pulmonary Institute (EXC 2026 project ID 390649896), and the European Molecular Biology Organization (EMBO) Young Investigator Programmees_ES
dc.language.isoenges_ES
dc.publisherAmerican Association for the Advancement of Science (AAAS) es_ES
dc.type.hasVersionAMes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.meshAnimals es_ES
dc.subject.meshEndothelium, Vascular es_ES
dc.subject.meshHEK293 Cells es_ES
dc.subject.meshHuman Umbilical Vein Endothelial Cells es_ES
dc.subject.meshHumans es_ES
dc.subject.meshMice es_ES
dc.subject.meshMice, Knockout es_ES
dc.subject.meshNeovascularization, Physiologic es_ES
dc.subject.meshProtein Domains es_ES
dc.subject.meshProtein Stability es_ES
dc.subject.meshRNA, Small Interfering es_ES
dc.subject.meshReceptor, Notch1 es_ES
dc.subject.meshSignal Transduction es_ES
dc.subject.meshUbiquitin Thiolesterase es_ES
dc.subject.meshProteolysis es_ES
dc.titleDeubiquitinase USP10 regulates Notch signaling in the endotheliumes_ES
dc.typejournal articlees_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.identifier.pubmedID30975888es_ES
dc.format.volume364es_ES
dc.format.number6436es_ES
dc.format.page188-193es_ES
dc.identifier.doi10.1126/science.aat0778es_ES
dc.contributor.funderMax Planck Society 
dc.contributor.funderUnión Europea. Comisión Europea. European Research Council (ERC) 
dc.contributor.funderDeutsche Forschungsgemeinschaft (Alemania) 
dc.contributor.funderGerman Centre for Cardiovascular Research 
dc.contributor.funderEuropean Molecular Biology Organization 
dc.description.peerreviewedes_ES
dc.identifier.e-issn1095-9203es_ES
dc.relation.publisherversionhttps://doi.org/10.1126/science.aat0778es_ES
dc.identifier.journalScience (New York, N.Y.)es_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Genética Molecular de la Angiogénesises_ES
dc.repisalud.institucionCNICes_ES
dc.rights.accessRightsopen accesses_ES


Ficheros en el ítem

Acceso Abierto
Thumbnail

Este ítem aparece en la(s) siguiente(s) colección(ones)

Mostrar el registro sencillo del ítem

Attribution-NonCommercial-NoDerivatives 4.0 Internacional
Este Item está sujeto a una licencia Creative Commons: Attribution-NonCommercial-NoDerivatives 4.0 Internacional