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