A single mutation in arrestin-2 prevents ERK1/2 activation by reducing c-Raf1 binding.
about
Analyzing the roles of multi-functional proteins in cells: The case of arrestins and GRKsThe effect of arrestin conformation on the recruitment of c-Raf1, MEK1, and ERK1/2 activationThe functional cycle of visual arrestins in photoreceptor cells.Different downstream signalling of CCK1 receptors regulates distinct functions of CCK in pancreatic beta cellsSilent scaffolds: inhibition OF c-Jun N-terminal kinase 3 activity in cell by dominant-negative arrestin-3 mutantManipulation of very few receptor discriminator residues greatly enhances receptor specificity of non-visual arrestinsArrestin 1 and Cone Arrestin 4 Have Unique Roles in Visual Function in an All-Cone Mouse Retina.Engineering visual arrestin-1 with special functional characteristicsJNK3 enzyme binding to arrestin-3 differentially affects the recruitment of upstream mitogen-activated protein (MAP) kinase kinasesSynthetic biology with surgical precision: targeted reengineering of signaling proteins.β-Arrestin-kinase scaffolds: turn them on or turn them off?Structural determinants of arrestin functionsExtensive shape shifting underlies functional versatility of arrestins.Arrestin-2 and arrestin-3 differentially modulate locomotor responses and sensitization to amphetamine.Depletion of β-arrestin2 in hepatic stellate cells reduces cell proliferation via ERK pathway.The Diverse Roles of Arrestin Scaffolds in G Protein-Coupled Receptor Signaling.Nonvisual arrestins function as simple scaffolds assembling the MKK4-JNK3α2 signaling complexTargeted Elimination of G Proteins and Arrestins Defines Their Specific Contributions to Both Intensity and Duration of G Protein-coupled Receptor Signaling.Unraveling the molecular architecture of a G protein-coupled receptor/β-arrestin/Erk module complex.Using Bioluminescence Resonance Energy Transfer (BRET) to Characterize Agonist-Induced Arrestin Recruitment to Modified and Unmodified G Protein-Coupled Receptors.Targeting individual GPCRs with redesigned nonvisual arrestins.Self-association of arrestin family members.Therapeutic potential of small molecules and engineered proteins.Arrestin-dependent activation of JNK family kinasesA synthetic intrabody-based selective and generic inhibitor of GPCR endocytosis.Lack of beta-arrestin signaling in the absence of active G proteins.
P2860
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P2860
A single mutation in arrestin-2 prevents ERK1/2 activation by reducing c-Raf1 binding.
description
2011 nî lūn-bûn
@nan
2011 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի հուլիսին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
A single mutation in arrestin-2 prevents ERK1/2 activation by reducing c-Raf1 binding.
@ast
A single mutation in arrestin-2 prevents ERK1/2 activation by reducing c-Raf1 binding.
@en
type
label
A single mutation in arrestin-2 prevents ERK1/2 activation by reducing c-Raf1 binding.
@ast
A single mutation in arrestin-2 prevents ERK1/2 activation by reducing c-Raf1 binding.
@en
prefLabel
A single mutation in arrestin-2 prevents ERK1/2 activation by reducing c-Raf1 binding.
@ast
A single mutation in arrestin-2 prevents ERK1/2 activation by reducing c-Raf1 binding.
@en
P2093
P2860
P356
P1433
P1476
A single mutation in arrestin-2 prevents ERK1/2 activation by reducing c-Raf1 binding
@en
P2093
Benjamin W Spiller
Maya Breitman
Sergio Coffa
P2860
P304
P356
10.1021/BI200745K
P407
P577
2011-07-13T00:00:00Z