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Statements

Subject Item
n2:RIV%2F00216224%3A14310%2F12%3A00065919%21RIV14-MSM-14310___
rdf:type
n9:Vysledek skos:Concept
dcterms:description
Beare-Stevenson cutis gyrata syndrome (BSS) is a human genetic disorder characterized by skin and skull abnormalities. BSS is caused by mutations in the FGF receptor 2 (FGFR2), but the molecular mechanisms that induce skin and skull abnormalities are unclear. We developed a mouse model of BSS harboring a FGFR2 Y394C mutation and identified p38 MAPK as an important signaling pathway mediating these abnormalities. Fgfr2+/Y394C mice exhibited epidermal hyperplasia and premature closure of cranial sutures (craniosynostosis) due to abnormal cell proliferation and differentiation. We found ligand-independent phosphorylation of FGFR2 and activation of p38 signaling in mutant skin and calvarial tissues. Treating Fgfr2+/Y394C mice with a p38 kinase inhibitor attenuated skin abnormalities by reversing cell proliferation and differentiation to near normal levels. Beare-Stevenson cutis gyrata syndrome (BSS) is a human genetic disorder characterized by skin and skull abnormalities. BSS is caused by mutations in the FGF receptor 2 (FGFR2), but the molecular mechanisms that induce skin and skull abnormalities are unclear. We developed a mouse model of BSS harboring a FGFR2 Y394C mutation and identified p38 MAPK as an important signaling pathway mediating these abnormalities. Fgfr2+/Y394C mice exhibited epidermal hyperplasia and premature closure of cranial sutures (craniosynostosis) due to abnormal cell proliferation and differentiation. We found ligand-independent phosphorylation of FGFR2 and activation of p38 signaling in mutant skin and calvarial tissues. Treating Fgfr2+/Y394C mice with a p38 kinase inhibitor attenuated skin abnormalities by reversing cell proliferation and differentiation to near normal levels.
dcterms:title
p38 Inhibition ameliorates skin and skull abnormalities in Fgfr2 Beare-Stevenson mice. p38 Inhibition ameliorates skin and skull abnormalities in Fgfr2 Beare-Stevenson mice.
skos:prefLabel
p38 Inhibition ameliorates skin and skull abnormalities in Fgfr2 Beare-Stevenson mice. p38 Inhibition ameliorates skin and skull abnormalities in Fgfr2 Beare-Stevenson mice.
skos:notation
RIV/00216224:14310/12:00065919!RIV14-MSM-14310___
n9:predkladatel
n21:orjk%3A14310
n3:aktivita
n5:Z n5:I n5:S n5:P
n3:aktivity
I, P(GA301/09/0587), P(GAP305/11/0752), S, Z(MSM0021622430)
n3:cisloPeriodika
6
n3:dodaniDat
n20:2014
n3:domaciTvurceVysledku
n12:5512646
n3:druhVysledku
n15:J
n3:duvernostUdaju
n11:S
n3:entitaPredkladatele
n14:predkladatel
n3:idSjednocenehoVysledku
163704
n3:idVysledku
RIV/00216224:14310/12:00065919
n3:jazykVysledku
n17:eng
n3:klicovaSlova
p38; skin; skull; FGFR2; Beare-Stevenson syndrome
n3:klicoveSlovo
n7:skin n7:p38 n7:FGFR2 n7:Beare-Stevenson%20syndrome n7:skull
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[327E245DFF4D]
n3:nazevZdroje
The Journal of Clinical Investigation
n3:obor
n19:ED
n3:pocetDomacichTvurcuVysledku
1
n3:pocetTvurcuVysledku
15
n3:projekt
n10:GA301%2F09%2F0587 n10:GAP305%2F11%2F0752
n3:rokUplatneniVysledku
n20:2012
n3:svazekPeriodika
122
n3:tvurceVysledku
Wang, Y. Oberoi, K. Richtsmeier, J. T. Couwenhoven, R. Huso, D. L. Rendl, Michael Wang Jabs, E. Zhou, X. Friedenthal, J. Rezza, A. Percival, Ch. J. Sun, M. Phelps, R. Holmes, G. Krejčí, Pavel
n3:wos
000304736300023
n3:zamer
n4:MSM0021622430
s:issn
0021-9738
s:numberOfPages
12
n16:doi
10.1172/JCI62644
n18:organizacniJednotka
14310