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Data show subfunctionalized expression of Arr3a in M- and L-cones, and Arr3b in S- and UV-cones, and suggest that Arr3a deficiency is sufficient to reduce temporal contrast sensitivity.
The G-protein coupled receptor, DRD4, requires ARR1 and ARR4 for desensitization and internalization.
Data indicate that In arrestin 3 (Montrer ARRB2 Anticorps) deficient mice, where the alpha2B (Montrer ADRA2B Anticorps) adrenergic receptor has a stronger binding to spinophilin (Montrer PPP1R9B Anticorps), the hypertensive response is enhanced.
rrestin-3 modulates the activity of ubiquitous JNK1 (Montrer MAPK8 Anticorps) and JNK2 (Montrer MAPK9 Anticorps) in non-neuronal cells, impacting the signaling pathway that regulates their proliferation and survival.
Arrestin-2 (Montrer ARRB1 Anticorps) and -3 association with beta(2)-adrenergic receptor (beta2AR (Montrer ADRB2 Anticorps)) significantly enhanced ERK2 (Montrer MAPK1 Anticorps) binding, but showed little effect on arrestin (Montrer SAG Anticorps) interactions with the upstream kinases c-Raf1 (Montrer RAF1 Anticorps) and MEK1 (Montrer MAP2K1 Anticorps).
of arrestin3 to the beta2-adrenergic receptor (Montrer ADRB2 Anticorps) orchestrates the sequestration of Gq-coupled receptor-induced ERK (Montrer EPHB2 Anticorps) to the cytosol through direct binding of ERK (Montrer EPHB2 Anticorps) to arrestin (Montrer SAG Anticorps).
Data demonstrate that the alpha(2A)AR (Montrer ADRA2A Anticorps) evokes ERK (Montrer EPHB2 Anticorps) phosphorylation through both an arrestin (Montrer SAG Anticorps)/Src (Montrer SRC Anticorps)-dependent and a Src (Montrer SRC Anticorps)-independent pathway, both of which are G protein dependent and converge on the Ras-Raf (Montrer RAF1 Anticorps)-MEK (Montrer MDK Anticorps) pathway.
These results demonstrate previously unknown crucial regulatory mechanisms that alter ARR/GRK expression levels in macrophages that might modify many, if not all, GPCR-mediated innate immune responses.
These results show that, in MA-10 cells, the hLHR activates Fyn (Montrer FYN Anticorps) through an arrestin-3 (Montrer ARRB2 Anticorps)-dependent pathway and that this pathway is a mediator of the hLHR-provoked release of EGF (Montrer EGF Anticorps)-like growth factors.
In the cell membrane, arrestin-3 (Montrer ARRB2 Anticorps) dissociates quickly and almost completely from the Beta2-adrenoceptor.
The 25-amino acid N-domain element of arrestin 3 (Montrer ARRB2 Anticorps) has the highest affinity for JNK3alpha2, suggesting that it is the key site for JNK3alpha2 docking.
arrestin-3 (Montrer ARRB2 Anticorps) regulates the activity of multiple JNK (Montrer MAPK8 Anticorps) isoforms, suggesting that it might play a role in survival and apoptosis of all cell types.
These data suggest cell type- and subcellular compartment-dependent differences in GRK (Montrer GRK4 Anticorps)/arrestin (Montrer SAG Anticorps)-mediated desensitization and signaling.
Silent scaffolds: inhibition OF c-Jun N-terminal kinase 3 (Montrer MAPK10 Anticorps) activity in cell by dominant-negative arrestin-3 (Montrer ARRB2 Anticorps) mutant.
the TGN (Montrer TG Anticorps) acts as a checkpoint for both the recycling and down-regulation of beta1AR (Montrer ADRB1 Anticorps) and arrestin-3 (Montrer ARRB2 Anticorps) not only mediates beta1AR (Montrer ADRB1 Anticorps) endocytosis but also its recycling through the TGN (Montrer TG Anticorps)
PP2A (Montrer PPP2R4 Anticorps) inhibits association between the Na+,K+-ATPase (Montrer ATP1A1 Anticorps) and arrestin (Montrer SAG Anticorps), and diminishes the effect of arrestin (Montrer SAG Anticorps) on Na+,K+-ATPase (Montrer ATP1A1 Anticorps) trafficking.
upon ligand activation, CysLT(1 (Montrer CYSLTR1 Anticorps))R is tyrosine-phosphorylated and released from heterodimers with CysLT(2 (Montrer CYSLTR2 Anticorps))R and, subsequently, internalizes from the plasma membrane to the nuclear membrane in a clathrin-, arrestin-3 (Montrer ARRB2 Anticorps)-, and Rab-5 (Montrer RAB5A Anticorps)-dependent manner
The agonist-induced internalization of GPR109A receptors is regulated by GRK2 (Montrer ADRBK1 Anticorps) and arrestin3 in a pertussis toxin-sensitive manner and that internalized receptor recycling is independent of endosomal acidification.
two non-visual arrestins, arrestin2 and arrestin3, localize to the centrosome, a key organelle involved in microtubule nucleation and bipolar mitotic spindle assembly
K2A mutations in arrestin-1 (Montrer SAG Anticorps), -2, and -3 significantly reduced their binding to active phosphorhodopsin.
multiple residues on the non-receptor-binding side of arrestin-3 (Montrer ARRB2 Anticorps) are crucial for JNK3 (Montrer MAPK10 Anticorps) activation
Both nonvisual arrestin-2 (Montrer ARRB1 Anticorps) and arrestin-3 (Montrer ARRB2 Anticorps) are shown to directly bind Jun kinase (JNK)3alpha2 and its upstream activator Map kinase (Montrer MAPK1 Anticorps) kinase (MKK)4 (Montrer MAP2K4 Anticorps); the affinity of arrestin-3 (Montrer ARRB2 Anticorps) for these kinases is higher than that of arrestin-2 (Montrer ARRB1 Anticorps).
the first crystal structure of arrestin-3 (Montrer ARRB2 Anticorps), solved at 3.0 A resolution. Receptor binding.
SUMOylation sites in arrestin-3 (Montrer ARRB2 Anticorps); arrestin-3 (Montrer ARRB2 Anticorps) SUMOylation mediates beta(2)AR internalization
The nature of the changes in arrestin 3 (Montrer ARRB2 Anticorps) distribution observed upon activation of adenosine receptors correlates with receptor sensitivity to G-protein-coupled receptor (Montrer GPBAR1 Anticorps) kinase-mediated phosphorylation and rapid internalization.
microtubule interaction may play a role in keeping p44 (Montrer GTF2H2 Anticorps) arrestin (Montrer SAG Anticorps) away from rhodopsin (Montrer RHO Anticorps) in dark-adapted photoreceptors
functions in deactivation of G protein-coupled receptors involved in color vision
arrestin 3, retinal (X-arrestin)
, cone arrestin
, arrestin 3, retinal
, arrestin 4
, retinal cone arrestin-3