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These data highlight a novel arrestin-mediated modulation of CREB signalling, suggesting a reciprocal relationship between arrestin2 and arrestin3, wherein recruitment of arrestin3 restricts the ability of beta2AR to activate prolonged CREB phosphorylation by precluding recruitment of an arrestin2/Src/p38 complex.
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These data suggest that heterozygous mutations in ARR3 might be responsible for X-linked female-limited early onset high myopia in the three families, a pattern contrary to the standard X-linked recessive trait.
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In the cell membrane, arrestin-3 dissociates quickly and almost completely from the Beta2-adrenoceptor.
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Identification of receptor binding-induced conformational changes in non-visual arrestins.
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The 25-amino acid N-domain element of arrestin 3 has the highest affinity for JNK3alpha2, suggesting that it is the key site for JNK3alpha2 docking.
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arrestin-3 regulates the activity of multiple JNK isoforms, suggesting that it might play a role in survival and apoptosis of all cell types.
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These data suggest cell type- and subcellular compartment-dependent differences in GRK/arrestin-mediated desensitization and signaling.
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Silent scaffolds: inhibition OF c-Jun N-terminal kinase 3 activity in cell by dominant-negative arrestin-3 mutant.
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the TGN acts as a checkpoint for both the recycling and down-regulation of beta1AR and arrestin-3 not only mediates beta1AR endocytosis but also its recycling through the TGN
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PP2A inhibits association between the Na+,K+-ATPase and arrestin, and diminishes the effect of arrestin on Na+,K+-ATPase trafficking.
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upon ligand activation, CysLT(1)R is tyrosine-phosphorylated and released from heterodimers with CysLT(2)R and, subsequently, internalizes from the plasma membrane to the nuclear membrane in a clathrin-, arrestin-3-, and Rab-5-dependent manner
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The agonist-induced internalization of GPR109A receptors is regulated by GRK2 and arrestin3 in a pertussis toxin-sensitive manner and that internalized receptor recycling is independent of endosomal acidification.
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two non-visual arrestins, arrestin2 and arrestin3, localize to the centrosome, a key organelle involved in microtubule nucleation and bipolar mitotic spindle assembly
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Regulation of arrestin-3 phosphorylation by casein kinase II.
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The light-dependent translocation of cone arrestin suggests a role in light-dark adaptation of cones.
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association of arrestin-3 with the FSHR is dependent on receptor phosphorylation, however phosphorylation of the third intracellular loop residues is not needed for arrestin-3 association.
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Autoimmunity to this antigen and retinal vasculitis is not altered in patients with Behcet's disease
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Arrestin in all conformations binds JNK3 comparably, whereas Mdm2 preferentially binds cone arrestin 'frozen' in the basal state.
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Arrestin 3 but not arrestin 2 is required for internalization of C-C chemokine receptor CCR7 when bound to C-C chemokine ligand CCL19. In contrast, arrestins are not required for internalization of CCR7/CCL21.
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the molecular interactions of arrestin2 and arrestin3 and their individual domains with the components of the two MAPK cascades, ASK1-MKK4-JNK3 and c-Raf-1-MEK1-ERK2