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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.
In the cell membrane, arrestin-3 (显示 ARRB2 抗体) dissociates quickly and almost completely from the Beta2-adrenoceptor.
The 25-amino acid N-domain element of arrestin 3 (显示 ARRB2 抗体) has the highest affinity for JNK3alpha2, suggesting that it is the key site for JNK3alpha2 docking.
arrestin-3 (显示 ARRB2 抗体) regulates the activity of multiple JNK (显示 MAPK8 抗体) 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 抗体)/arrestin (显示 SAG 抗体)-mediated desensitization and signaling.
Silent scaffolds: inhibition OF c-Jun N-terminal kinase 3 (显示 MAPK10 抗体) activity in cell by dominant-negative arrestin-3 (显示 ARRB2 抗体) mutant.
the TGN (显示 TG 抗体) acts as a checkpoint for both the recycling and down-regulation of beta1AR (显示 ADRB1 抗体) and arrestin-3 (显示 ARRB2 抗体) not only mediates beta1AR (显示 ADRB1 抗体) endocytosis but also its recycling through the TGN (显示 TG 抗体)
PP2A (显示 PPP2R4 抗体) inhibits association between the Na+,K+-ATPase (显示 ATP1A1 抗体) and arrestin (显示 SAG 抗体), and diminishes the effect of arrestin (显示 SAG 抗体) on Na+,K+-ATPase (显示 ATP1A1 抗体) trafficking.
upon ligand activation, CysLT(1 (显示 CYSLTR1 抗体))R is tyrosine-phosphorylated and released from heterodimers with CysLT(2 (显示 CYSLTR2 抗体))R and, subsequently, internalizes from the plasma membrane to the nuclear membrane in a clathrin-, arrestin-3 (显示 ARRB2 抗体)-, and Rab-5 (显示 RAB5A 抗体)-dependent manner
The agonist-induced internalization of GPR109A (显示 HCAR2 抗体) receptors is regulated by GRK2 (显示 ADRBK1 抗体) and arrestin3 in a pertussis toxin-sensitive manner and that internalized receptor recycling is independent of endosomal acidification.
The G-protein coupled receptor, DRD4, requires ARR1 and ARR4 for desensitization and internalization.
Data indicate that In arrestin 3 (显示 ARRB2 抗体) deficient mice, where the alpha2B (显示 ADRA2B 抗体) adrenergic receptor has a stronger binding to spinophilin (显示 PPP1R9B 抗体), the hypertensive response is enhanced.
rrestin-3 modulates the activity of ubiquitous JNK1 (显示 MAPK8 抗体) and JNK2 (显示 MAPK9 抗体) in non-neuronal cells, impacting the signaling pathway that regulates their proliferation and survival.
Arrestin-2 (显示 ARRB1 抗体) and -3 association with beta(2)-adrenergic receptor (beta2AR (显示 ADRB2 抗体)) significantly enhanced ERK2 (显示 MAPK1 抗体) binding, but showed little effect on arrestin (显示 SAG 抗体) interactions with the upstream kinases c-Raf1 (显示 RAF1 抗体) and MEK1 (显示 MAP2K1 抗体).
of arrestin3 to the beta2-adrenergic receptor (显示 ADRB2 抗体) orchestrates the sequestration of Gq-coupled receptor-induced ERK (显示 EPHB2 抗体) to the cytosol through direct binding of ERK (显示 EPHB2 抗体) to arrestin (显示 SAG 抗体).
Data demonstrate that the alpha(2A)AR (显示 ADRA2A 抗体) evokes ERK (显示 EPHB2 抗体) phosphorylation through both an arrestin (显示 SAG 抗体)/Src (显示 SRC 抗体)-dependent and a Src (显示 SRC 抗体)-independent pathway, both of which are G protein dependent and converge on the Ras-Raf (显示 RAF1 抗体)-MEK (显示 MDK 抗体) 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 抗体) through an arrestin-3 (显示 ARRB2 抗体)-dependent pathway and that this pathway is a mediator of the hLHR-provoked release of EGF (显示 EGF 抗体)-like growth factors.
Several mutations in the two parts of the central "crest" of the arrestin (显示 SAG 抗体) molecule, middle-loop and C-loop, enhanced or reduced arrestin-3 (显示 ARRB2 抗体) interactions with several GPCRs in receptor subtype and functional state-specific manner.
K2A mutations in arrestin-1 (显示 SAG 抗体), -2, and -3 significantly reduced their binding to active phosphorhodopsin.
multiple residues on the non-receptor-binding side of arrestin-3 (显示 ARRB2 抗体) are crucial for JNK3 (显示 MAPK10 抗体) activation
Both nonvisual arrestin-2 (显示 ARRB1 抗体) and arrestin-3 (显示 ARRB2 抗体) are shown to directly bind Jun kinase (JNK)3alpha2 and its upstream activator Map kinase (显示 MAPK1 抗体) kinase (MKK)4 (显示 MAP2K4 抗体); the affinity of arrestin-3 (显示 ARRB2 抗体) for these kinases is higher than that of arrestin-2 (显示 ARRB1 抗体).
the first crystal structure of arrestin-3 (显示 ARRB2 抗体), solved at 3.0 A resolution. Receptor binding.
SUMOylation sites in arrestin-3 (显示 ARRB2 抗体); arrestin-3 (显示 ARRB2 抗体) SUMOylation mediates beta(2)AR internalization
The nature of the changes in arrestin 3 (显示 ARRB2 抗体) distribution observed upon activation of adenosine receptors correlates with receptor sensitivity to G-protein-coupled receptor (显示 GPBAR1 抗体) kinase-mediated phosphorylation and rapid internalization.
microtubule interaction may play a role in keeping p44 (显示 GTF2H2 抗体) arrestin (显示 SAG 抗体) away from rhodopsin (显示 RHO 抗体) in dark-adapted photoreceptors
functions in deactivation of G protein-coupled receptors involved in color vision
, arrestin 4
, cone arrestin
, retinal cone arrestin-3
, arrestin 3, retinal (X-arrestin)
, arrestin 3, retinal