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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 (show ARRB2 ELISA Kits) deficient mice, where the alpha2B (show ADRA2B ELISA Kits) adrenergic receptor has a stronger binding to spinophilin (show PPP1R9B ELISA Kits), the hypertensive response is enhanced.
rrestin-3 modulates the activity of ubiquitous JNK1 (show MAPK8 ELISA Kits) and JNK2 (show MAPK9 ELISA Kits) in non-neuronal cells, impacting the signaling pathway that regulates their proliferation and survival.
Arrestin-2 (show ARRB1 ELISA Kits) and -3 association with beta(2)-adrenergic receptor (beta2AR (show ADRB2 ELISA Kits)) significantly enhanced ERK2 (show MAPK1 ELISA Kits) binding, but showed little effect on arrestin (show SAG ELISA Kits) interactions with the upstream kinases c-Raf1 (show RAF1 ELISA Kits) and MEK1 (show MAP2K1 ELISA Kits).
of arrestin3 to the beta2-adrenergic receptor (show ADRB2 ELISA Kits) orchestrates the sequestration of Gq-coupled receptor-induced ERK (show EPHB2 ELISA Kits) to the cytosol through direct binding of ERK (show EPHB2 ELISA Kits) to arrestin (show SAG ELISA Kits).
Data demonstrate that the alpha(2A)AR (show ADRA2A ELISA Kits) evokes ERK (show EPHB2 ELISA Kits) phosphorylation through both an arrestin (show SAG ELISA Kits)/Src (show SRC ELISA Kits)-dependent and a Src (show SRC ELISA Kits)-independent pathway, both of which are G protein dependent and converge on the Ras-Raf (show RAF1 ELISA Kits)-MEK (show MDK ELISA Kits) 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 (show FYN ELISA Kits) through an arrestin-3 (show ARRB2 ELISA Kits)-dependent pathway and that this pathway is a mediator of the hLHR-provoked release of EGF (show EGF ELISA Kits)-like growth factors.
In the cell membrane, arrestin-3 (show ARRB2 ELISA Kits) dissociates quickly and almost completely from the Beta2-adrenoceptor.
The 25-amino acid N-domain element of arrestin 3 (show ARRB2 ELISA Kits) has the highest affinity for JNK3alpha2, suggesting that it is the key site for JNK3alpha2 docking.
arrestin-3 (show ARRB2 ELISA Kits) regulates the activity of multiple JNK (show MAPK8 ELISA Kits) 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 (show GRK4 ELISA Kits)/arrestin (show SAG ELISA Kits)-mediated desensitization and signaling.
Silent scaffolds: inhibition OF c-Jun N-terminal kinase 3 (show MAPK10 ELISA Kits) activity in cell by dominant-negative arrestin-3 (show ARRB2 ELISA Kits) mutant.
the TGN (show TG ELISA Kits) acts as a checkpoint for both the recycling and down-regulation of beta1AR (show ADRB1 ELISA Kits) and arrestin-3 (show ARRB2 ELISA Kits) not only mediates beta1AR (show ADRB1 ELISA Kits) endocytosis but also its recycling through the TGN (show TG ELISA Kits)
PP2A (show PPP2R4 ELISA Kits) inhibits association between the Na+,K+-ATPase (show ATP1A1 ELISA Kits) and arrestin (show SAG ELISA Kits), and diminishes the effect of arrestin (show SAG ELISA Kits) on Na+,K+-ATPase (show ATP1A1 ELISA Kits) trafficking.
upon ligand activation, CysLT(1 (show CYSLTR1 ELISA Kits))R is tyrosine-phosphorylated and released from heterodimers with CysLT(2 (show CYSLTR2 ELISA Kits))R and, subsequently, internalizes from the plasma membrane to the nuclear membrane in a clathrin-, arrestin-3 (show ARRB2 ELISA Kits)-, and Rab-5 (show RAB5A ELISA Kits)-dependent manner
The agonist-induced internalization of GPR109A receptors is regulated by GRK2 (show ADRBK1 ELISA Kits) 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 (show SAG ELISA Kits), -2, and -3 significantly reduced their binding to active phosphorhodopsin.
multiple residues on the non-receptor-binding side of arrestin-3 (show ARRB2 ELISA Kits) are crucial for JNK3 (show MAPK10 ELISA Kits) activation
Both nonvisual arrestin-2 (show ARRB1 ELISA Kits) and arrestin-3 (show ARRB2 ELISA Kits) are shown to directly bind Jun kinase (JNK)3alpha2 and its upstream activator Map kinase (show MAPK1 ELISA Kits) kinase (MKK)4 (show MAP2K4 ELISA Kits); the affinity of arrestin-3 (show ARRB2 ELISA Kits) for these kinases is higher than that of arrestin-2 (show ARRB1 ELISA Kits).
the first crystal structure of arrestin-3 (show ARRB2 ELISA Kits), solved at 3.0 A resolution. Receptor binding.
SUMOylation sites in arrestin-3 (show ARRB2 ELISA Kits); arrestin-3 (show ARRB2 ELISA Kits) SUMOylation mediates beta(2)AR internalization
The nature of the changes in arrestin 3 (show ARRB2 ELISA Kits) distribution observed upon activation of adenosine receptors correlates with receptor sensitivity to G-protein-coupled receptor (show GPBAR1 ELISA Kits) kinase-mediated phosphorylation and rapid internalization.
microtubule interaction may play a role in keeping p44 (show GTF2H2 ELISA Kits) arrestin (show SAG ELISA Kits) away from rhodopsin (show RHO ELISA Kits) 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