Noonan syndrome mutation Q79R in Shp2 increases proliferation of valve primordia mesenchymal cells via extracellular signal-regulated kinase 1/2 signaling.
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Functional effects of PTPN11 (SHP2) mutations causing LEOPARD syndrome on epidermal growth factor-induced phosphoinositide 3-kinase/AKT/glycogen synthase kinase 3beta signalingMEKK3 initiates transforming growth factor beta 2-dependent epithelial-to-mesenchymal transition during endocardial cushion morphogenesisPaternal age effect mutations and selfish spermatogonial selection: causes and consequences for human diseasePTPN11 (Shp2) mutations in LEOPARD syndrome have dominant negative, not activating, effectsMitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale.Optical coherence tomography captures rapid hemodynamic responses to acute hypoxia in the cardiovascular system of early embryos.Structural insights into Noonan/LEOPARD syndrome-related mutants of protein-tyrosine phosphatase SHP2 (PTPN11)The Q510E mutation in Shp2 perturbs heart valve development by increasing cell migration.Xenopus: An emerging model for studying congenital heart disease.Mediating ERK 1/2 signaling rescues congenital heart defects in a mouse model of Noonan syndrome.Ras-related signaling pathways in valve development: ebb and flow.Atrioventricular canal defect in patients with RASopathies.Wnt/β-catenin signaling enables developmental transitions during valvulogenesis.Genetic approaches for changing the heart and dissecting complex syndromes.Mitogen-activated protein kinases in heart development and diseasesRole of ERK1/2 signaling in congenital valve malformations in Noonan syndromeNoonan syndrome cardiac defects are caused by PTPN11 acting in endocardium to enhance endocardial-mesenchymal transformation.Tgfβ-Smad and MAPK signaling mediate scleraxis and proteoglycan expression in heart valves.Heart valve development: regulatory networks in development and diseaseMolecular and developmental mechanisms of congenital heart valve disease.How to make a heart valve: from embryonic development to bioengineering of living valve substitutes.Noonan syndrome-associated SHP-2/Ptpn11 mutants enhance SIRPalpha and PZR tyrosyl phosphorylation and promote adhesion-mediated ERK activationNew approaches to prevent LEOPARD syndrome-associated cardiac hypertrophy by specifically targeting Shp2-dependent signaling.VEGF and RANKL regulation of NFATc1 in heart valve development.The FGF-BMP signaling axis regulates outflow tract valve primordium formation by promoting cushion neural crest cell differentiation.Congenital heart disease and genetic syndromes: new insights into molecular mechanisms.MEKK4 regulates developmental EMT in the embryonic heart.
P2860
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P2860
Noonan syndrome mutation Q79R in Shp2 increases proliferation of valve primordia mesenchymal cells via extracellular signal-regulated kinase 1/2 signaling.
description
2005 nî lūn-bûn
@nan
2005 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2005 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
name
Noonan syndrome mutation Q79R ...... egulated kinase 1/2 signaling.
@ast
Noonan syndrome mutation Q79R ...... egulated kinase 1/2 signaling.
@en
Noonan syndrome mutation Q79R ...... egulated kinase 1/2 signaling.
@nl
type
label
Noonan syndrome mutation Q79R ...... egulated kinase 1/2 signaling.
@ast
Noonan syndrome mutation Q79R ...... egulated kinase 1/2 signaling.
@en
Noonan syndrome mutation Q79R ...... egulated kinase 1/2 signaling.
@nl
prefLabel
Noonan syndrome mutation Q79R ...... egulated kinase 1/2 signaling.
@ast
Noonan syndrome mutation Q79R ...... egulated kinase 1/2 signaling.
@en
Noonan syndrome mutation Q79R ...... egulated kinase 1/2 signaling.
@nl
P2860
P1433
P1476
Noonan syndrome mutation Q79R ...... regulated kinase 1/2 signaling
@en
P2093
Jeffrey Robbins
Maike Krenz
P2860
P304
P356
10.1161/01.RES.0000186194.06514.B0
P577
2005-09-15T00:00:00Z