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Oligodendrocyte-specific deletion of FGFR2 ameliorates MOG35-55-induced EAE through ERK and Akt signalling

dc.contributor.authorKamali, Salar
dc.contributor.authorRajendran, Ranjithkumar
dc.contributor.authorStadelmann, Christine
dc.contributor.authorKarnati, Srikanth
dc.contributor.authorRajendran, Vinothkumar
dc.contributor.authorGiraldo-Velasquez, Mario
dc.contributor.authorBerghoff, Martin
dc.date.accessioned2022-09-05T12:24:22Z
dc.date.available2022-09-05T12:24:22Z
dc.date.issued2021
dc.identifier.urihttps://jlupub.ub.uni-giessen.de//handle/jlupub/7386
dc.identifier.urihttp://dx.doi.org/10.22029/jlupub-6837
dc.language.isoen
dc.rightsNamensnennung 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subject.ddcddc:610
dc.titleOligodendrocyte-specific deletion of FGFR2 ameliorates MOG35-55-induced EAE through ERK and Akt signalling
dc.typearticle
local.affiliationFB 11 - Medizin
local.source.spage297
local.source.epage311
local.source.journaltitleBrain pathology
local.source.volume31
local.source.urihttps://doi.org/10.1111/bpa.12916


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