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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 (显示 ARRB2 ELISA试剂盒) deficient mice, where the alpha2B (显示 ADRA2B ELISA试剂盒) adrenergic receptor has a stronger binding to spinophilin (显示 PPP1R9B ELISA试剂盒), the hypertensive response is enhanced.
rrestin-3 modulates the activity of ubiquitous JNK1 (显示 MAPK8 ELISA试剂盒) and JNK2 (显示 MAPK9 ELISA试剂盒) in non-neuronal cells, impacting the signaling pathway that regulates their proliferation and survival.
Arrestin-2 (显示 ARRB1 ELISA试剂盒) and -3 association with beta(2)-adrenergic receptor (beta2AR (显示 ADRB2 ELISA试剂盒)) significantly enhanced ERK2 (显示 MAPK1 ELISA试剂盒) binding, but showed little effect on arrestin (显示 SAG ELISA试剂盒) interactions with the upstream kinases c-Raf1 (显示 RAF1 ELISA试剂盒) and MEK1 (显示 MAP2K1 ELISA试剂盒).
of arrestin3 to the beta2-adrenergic receptor (显示 ADRB2 ELISA试剂盒) orchestrates the sequestration of Gq-coupled receptor-induced ERK (显示 EPHB2 ELISA试剂盒) to the cytosol through direct binding of ERK (显示 EPHB2 ELISA试剂盒) to arrestin (显示 SAG ELISA试剂盒).
Data demonstrate that the alpha(2A)AR (显示 ADRA2A ELISA试剂盒) evokes ERK (显示 EPHB2 ELISA试剂盒) phosphorylation through both an arrestin (显示 SAG ELISA试剂盒)/Src (显示 SRC ELISA试剂盒)-dependent and a Src (显示 SRC ELISA试剂盒)-independent pathway, both of which are G protein dependent and converge on the Ras-Raf (显示 RAF1 ELISA试剂盒)-MEK (显示 MDK ELISA试剂盒) 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 (显示 FYN ELISA试剂盒) through an arrestin-3 (显示 ARRB2 ELISA试剂盒)-dependent pathway and that this pathway is a mediator of the hLHR-provoked release of EGF (显示 EGF ELISA试剂盒)-like growth factors.
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.
In the cell membrane, arrestin-3 (显示 ARRB2 ELISA试剂盒) dissociates quickly and almost completely from the Beta2-adrenoceptor.
The 25-amino acid N-domain element of arrestin 3 (显示 ARRB2 ELISA试剂盒) has the highest affinity for JNK3alpha2, suggesting that it is the key site for JNK3alpha2 docking.
arrestin-3 (显示 ARRB2 ELISA试剂盒) regulates the activity of multiple JNK (显示 MAPK8 ELISA试剂盒) 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 (显示 GRK4 ELISA试剂盒)/arrestin (显示 SAG ELISA试剂盒)-mediated desensitization and signaling.
Silent scaffolds: inhibition OF c-Jun N-terminal kinase 3 (显示 MAPK10 ELISA试剂盒) activity in cell by dominant-negative arrestin-3 (显示 ARRB2 ELISA试剂盒) mutant.
the TGN (显示 TG ELISA试剂盒) acts as a checkpoint for both the recycling and down-regulation of beta1AR (显示 ADRB1 ELISA试剂盒) and arrestin-3 (显示 ARRB2 ELISA试剂盒) not only mediates beta1AR (显示 ADRB1 ELISA试剂盒) endocytosis but also its recycling through the TGN (显示 TG ELISA试剂盒)
PP2A (显示 PPP2R4 ELISA试剂盒) inhibits association between the Na+,K+-ATPase (显示 ATP1A1 ELISA试剂盒) and arrestin (显示 SAG ELISA试剂盒), and diminishes the effect of arrestin (显示 SAG ELISA试剂盒) on Na+,K+-ATPase (显示 ATP1A1 ELISA试剂盒) trafficking.
upon ligand activation, CysLT(1 (显示 CYSLTR1 ELISA试剂盒))R is tyrosine-phosphorylated and released from heterodimers with CysLT(2 (显示 CYSLTR2 ELISA试剂盒))R and, subsequently, internalizes from the plasma membrane to the nuclear membrane in a clathrin-, arrestin-3 (显示 ARRB2 ELISA试剂盒)-, and Rab-5 (显示 RAB5A ELISA试剂盒)-dependent manner
The agonist-induced internalization of GPR109A receptors is regulated by GRK2 (显示 ADRBK1 ELISA试剂盒) and arrestin3 in a pertussis toxin-sensitive manner and that internalized receptor recycling is independent of endosomal acidification.
K2A mutations in arrestin-1 (显示 SAG ELISA试剂盒), -2, and -3 significantly reduced their binding to active phosphorhodopsin.
multiple residues on the non-receptor-binding side of arrestin-3 (显示 ARRB2 ELISA试剂盒) are crucial for JNK3 (显示 MAPK10 ELISA试剂盒) activation
Both nonvisual arrestin-2 (显示 ARRB1 ELISA试剂盒) and arrestin-3 (显示 ARRB2 ELISA试剂盒) are shown to directly bind Jun kinase (JNK)3alpha2 and its upstream activator Map kinase (显示 MAPK1 ELISA试剂盒) kinase (MKK)4 (显示 MAP2K4 ELISA试剂盒); the affinity of arrestin-3 (显示 ARRB2 ELISA试剂盒) for these kinases is higher than that of arrestin-2 (显示 ARRB1 ELISA试剂盒).
the first crystal structure of arrestin-3 (显示 ARRB2 ELISA试剂盒), solved at 3.0 A resolution. Receptor binding.
SUMOylation sites in arrestin-3 (显示 ARRB2 ELISA试剂盒); arrestin-3 (显示 ARRB2 ELISA试剂盒) SUMOylation mediates beta(2)AR internalization
The nature of the changes in arrestin 3 (显示 ARRB2 ELISA试剂盒) distribution observed upon activation of adenosine receptors correlates with receptor sensitivity to G-protein-coupled receptor (显示 GPBAR1 ELISA试剂盒) kinase-mediated phosphorylation and rapid internalization.
microtubule interaction may play a role in keeping p44 (显示 GTF2H2 ELISA试剂盒) arrestin (显示 SAG ELISA试剂盒) away from rhodopsin (显示 RHO ELISA试剂盒) 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