000120520 001__ 120520
000120520 005__ 20240228145450.0
000120520 0247_ $$2doi$$a10.1084/jem.20160311
000120520 0247_ $$2pmid$$apmid:28289053
000120520 0247_ $$2pmc$$apmc:PMC5379968
000120520 0247_ $$2ISSN$$a0022-1007
000120520 0247_ $$2ISSN$$a1540-9538
000120520 0247_ $$2altmetric$$aaltmetric:17408992
000120520 037__ $$aDKFZ-2017-00949
000120520 041__ $$aeng
000120520 082__ $$a610
000120520 1001_ $$aFantin, Alessandro$$b0
000120520 245__ $$aVEGF165-induced vascular permeability requires NRP1 for ABL-mediated SRC family kinase activation.
000120520 260__ $$aNew York, NY$$bRockefeller Univ. Press$$c2017
000120520 3367_ $$2DRIVER$$aarticle
000120520 3367_ $$2DataCite$$aOutput Types/Journal article
000120520 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1524654446_18387
000120520 3367_ $$2BibTeX$$aARTICLE
000120520 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000120520 3367_ $$00$$2EndNote$$aJournal Article
000120520 520__ $$aThe vascular endothelial growth factor (VEGF) isoform VEGF165 stimulates vascular growth and hyperpermeability. Whereas blood vessel growth is essential to sustain organ health, chronic hyperpermeability causes damaging tissue edema. By combining in vivo and tissue culture models, we show here that VEGF165-induced vascular leakage requires both VEGFR2 and NRP1, including the VEGF164-binding site of NRP1 and the NRP1 cytoplasmic domain (NCD), but not the known NCD interactor GIPC1. In the VEGF165-bound receptor complex, the NCD promotes ABL kinase activation, which in turn is required to activate VEGFR2-recruited SRC family kinases (SFKs). These results elucidate the receptor complex and signaling hierarchy of downstream kinases that transduce the permeability response to VEGF165. In a mouse model with choroidal neovascularisation akin to age-related macular degeneration, NCD loss attenuated vessel leakage without affecting neovascularisation. These findings raise the possibility that targeting NRP1 or its NCD interactors may be a useful therapeutic strategy in neovascular disease to reduce VEGF165-induced edema without compromising vessel growth.
000120520 536__ $$0G:(DE-HGF)POF3-321$$a321 - Basic Concepts (POF3-321)$$cPOF3-321$$fPOF III$$x0
000120520 588__ $$aDataset connected to CrossRef, PubMed,
000120520 7001_ $$aLampropoulou, Anastasia$$b1
000120520 7001_ $$aSenatore, Valentina$$b2
000120520 7001_ $$aBrash, James T$$b3
000120520 7001_ $$00000-0002-6412-1907$$aPrahst, Claudia$$b4
000120520 7001_ $$00000-0002-2580-6823$$aLange, Clemens A$$b5
000120520 7001_ $$aLiyanage, Sidath E$$b6
000120520 7001_ $$aRaimondi, Claudio$$b7
000120520 7001_ $$aBainbridge, James W$$b8
000120520 7001_ $$00000-0002-7173-4242$$aAugustin, Hellmut G$$b9
000120520 7001_ $$00000-0002-3212-9381$$aRuhrberg, Christiana$$b10
000120520 773__ $$0PERI:(DE-600)1477240-1$$a10.1084/jem.20160311$$gVol. 214, no. 4, p. 1049 - 1064$$n4$$p1049 - 1064$$tJournal of experimental medicine$$v214$$x1540-9538$$y2017
000120520 909CO $$ooai:inrepo02.dkfz.de:120520$$pVDB
000120520 9101_ $$0I:(DE-588b)2036810-0$$60000-0002-7173-4242$$aDeutsches Krebsforschungszentrum$$b9$$kDKFZ
000120520 9131_ $$0G:(DE-HGF)POF3-321$$1G:(DE-HGF)POF3-320$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lHerz-Kreislauf-Stoffwechselerkrankungen$$vBasic Concepts$$x0
000120520 9141_ $$y2017
000120520 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline
000120520 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database
000120520 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bJ EXP MED : 2015
000120520 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS
000120520 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bThomson Reuters Master Journal List
000120520 915__ $$0StatID:(DE-HGF)0110$$2StatID$$aWoS$$bScience Citation Index
000120520 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection
000120520 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded
000120520 915__ $$0StatID:(DE-HGF)1030$$2StatID$$aDBCoverage$$bCurrent Contents - Life Sciences
000120520 915__ $$0StatID:(DE-HGF)1050$$2StatID$$aDBCoverage$$bBIOSIS Previews
000120520 915__ $$0StatID:(DE-HGF)9910$$2StatID$$aIF >= 10$$bJ EXP MED : 2015
000120520 9201_ $$0I:(DE-He78)A190-20160331$$kA190$$lVaskuläre Onkologie und Metastasierung$$x0
000120520 980__ $$ajournal
000120520 980__ $$aVDB
000120520 980__ $$aI:(DE-He78)A190-20160331
000120520 980__ $$aUNRESTRICTED