Binding of laminin alpha1-chain LG4-5 domain to alpha-dystroglycan causes tyrosine phosphorylation of syntrophin to initiate Rac1 signaling.
about
Interaction of alpha1-syntrophin with multiple isoforms of heterotrimeric G protein alpha subunitsThe conserved WW-domain binding sites in Dystroglycan C-terminus are essential but partially redundant for Dystroglycan functionA putative Src homology 3 domain binding motif but not the C-terminal dystrophin WW domain binding motif is required for dystroglycan function in cellular polarity in Drosophila.Rac1 is essential for basement membrane-dependent epiblast survivalDystrophin glycoprotein complex-associated Gbetagamma subunits activate phosphatidylinositol-3-kinase/Akt signaling in skeletal muscle in a laminin-dependent manner.MicroRNA-486-dependent modulation of DOCK3/PTEN/AKT signaling pathways improves muscular dystrophy-associated symptomsAltered expression of natively glycosylated alpha dystroglycan in pediatric solid tumors.Dg-Dys-Syn1 signaling in Drosophila regulates the microRNA profilePhosphorylation within the cysteine-rich region of dystrophin enhances its association with β-dystroglycan and identifies a potential novel therapeutic target for skeletal muscle wasting.Basement membranes: cell scaffoldings and signaling platforms.Laminin-α1 LG4-5 domain binding to dystroglycan mediates muscle cell survival, growth, and the AP-1 and NF-κB transcription factors but also has adverse effects.Dystroglycan expression in human placenta: basement membrane localization and subunit distribution change between the first and third trimesterAbsence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Polarization and myelination in myelinating glia.The congenital muscular dystrophies: recent advances and molecular insights.Laminin-induced activation of Rac1 and JNKp46 is initiated by Src family kinases and mimics the effects of skeletal muscle contractionMuscular dystrophy associated with alpha-dystroglycan deficiency in Sphynx and Devon Rex cats.The synaptic CT carbohydrate modulates binding and expression of extracellular matrix proteins in skeletal muscle: Partial dependence on utrophin.Stress-induced ECM alteration modulates cellular microRNAs that feedback to readjust the extracellular environment and cell behavior.Hyperthermic seizures and aberrant cellular homeostasis in Drosophila dystrophic muscles.LG4-5 domains of laminin-211 binds alpha-dystroglycan to allow myotube attachment and prevent anoikis.
P2860
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P2860
Binding of laminin alpha1-chain LG4-5 domain to alpha-dystroglycan causes tyrosine phosphorylation of syntrophin to initiate Rac1 signaling.
description
2006 nî lūn-bûn
@nan
2006 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
name
Binding of laminin alpha1-chai ...... in to initiate Rac1 signaling.
@ast
Binding of laminin alpha1-chai ...... in to initiate Rac1 signaling.
@en
type
label
Binding of laminin alpha1-chai ...... in to initiate Rac1 signaling.
@ast
Binding of laminin alpha1-chai ...... in to initiate Rac1 signaling.
@en
prefLabel
Binding of laminin alpha1-chai ...... in to initiate Rac1 signaling.
@ast
Binding of laminin alpha1-chai ...... in to initiate Rac1 signaling.
@en
P2093
P356
P1433
P1476
Binding of laminin alpha1-chai ...... in to initiate Rac1 signaling.
@en
P2093
Donald Gullberg
Harry W Jarrett
Yan Wen Zhou
P304
P356
10.1021/BI0519957
P407
P577
2006-02-01T00:00:00Z