Aperçu des produits pour anti-Arrestin 3, Retinal (X-Arrestin) (ARR3) Anticorps

Human Arrestin 3, Retinal (X-Arrestin) (ARR3) interaction partners

1. >15-fold higher affinity for inactive JNK3 than for active JNK3; shift in the binding site following JNK3 activation

2. These data highlight a novel arrestin-mediated modulation of CREB signalling, suggesting a reciprocal relationship between arrestin2 and arrestin3, wherein recruitment of arrestin3 restricts the ability of beta2AR to activate prolonged CREB phosphorylation by precluding recruitment of an arrestin2/Src/p38 complex.

3. 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.

4. In the cell membrane, arrestin-3 dissociates quickly and almost completely from the Beta2-adrenoceptor.

5. Identification of receptor binding-induced conformational changes in non-visual arrestins.

6. The 25-amino acid N-domain element of arrestin 3 has the highest affinity for JNK3alpha2, suggesting that it is the key site for JNK3alpha2 docking.

7. arrestin-3 regulates the activity of multiple JNK isoforms, suggesting that it might play a role in survival and apoptosis of all cell types.

8. These data suggest cell type- and subcellular compartment-dependent differences in GRK/arrestin-mediated desensitization and signaling.

9. Silent scaffolds: inhibition OF c-Jun N-terminal kinase 3 activity in cell by dominant-negative arrestin-3 mutant.

10. the TGN acts as a checkpoint for both the recycling and down-regulation of beta1AR and arrestin-3 not only mediates beta1AR endocytosis but also its recycling through the TGN

11. PP2A inhibits association between the Na+,K+-ATPase and arrestin, and diminishes the effect of arrestin on Na+,K+-ATPase trafficking.

12. upon ligand activation, CysLT(1)R is tyrosine-phosphorylated and released from heterodimers with CysLT(2)R and, subsequently, internalizes from the plasma membrane to the nuclear membrane in a clathrin-, arrestin-3-, and Rab-5-dependent manner

13. The agonist-induced internalization of GPR109A receptors is regulated by GRK2 and arrestin3 in a pertussis toxin-sensitive manner and that internalized receptor recycling is independent of endosomal acidification.

14. two non-visual arrestins, arrestin2 and arrestin3, localize to the centrosome, a key organelle involved in microtubule nucleation and bipolar mitotic spindle assembly

15. Regulation of arrestin-3 phosphorylation by casein kinase II.

16. The light-dependent translocation of cone arrestin suggests a role in light-dark adaptation of cones.

17. association of arrestin-3 with the FSHR is dependent on receptor phosphorylation, however phosphorylation of the third intracellular loop residues is not needed for arrestin-3 association.

18. Autoimmunity to this antigen and retinal vasculitis is not altered in patients with Behcet's disease

19. Arrestin in all conformations binds JNK3 comparably, whereas Mdm2 preferentially binds cone arrestin 'frozen' in the basal state.

20. Arrestin 3 but not arrestin 2 is required for internalization of C-C chemokine receptor CCR7 when bound to C-C chemokine ligand CCL19. In contrast, arrestins are not required for internalization of CCR7/CCL21.

Zebrafish Arrestin 3, Retinal (X-Arrestin) (ARR3) interaction partners

1. 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.

Mouse (Murine) Arrestin 3, Retinal (X-Arrestin) (ARR3) interaction partners

1. The G-protein coupled receptor, DRD4, requires ARR1 and ARR4 for desensitization and internalization.

2. Data indicate that In arrestin 3 deficient mice, where the alpha2B adrenergic receptor has a stronger binding to spinophilin, the hypertensive response is enhanced.

3. rrestin-3 modulates the activity of ubiquitous JNK1 and JNK2 in non-neuronal cells, impacting the signaling pathway that regulates their proliferation and survival.

4. Arrestin-2 and -3 association with beta(2)-adrenergic receptor (beta2AR) significantly enhanced ERK2 binding, but showed little effect on arrestin interactions with the upstream kinases c-Raf1 and MEK1.

5. of arrestin3 to the beta2-adrenergic receptor orchestrates the sequestration of Gq-coupled receptor-induced ERK to the cytosol through direct binding of ERK to arrestin.

6. Data demonstrate that the alpha(2A)AR evokes ERK phosphorylation through both an arrestin/Src-dependent and a Src-independent pathway, both of which are G protein dependent and converge on the Ras-Raf-MEK pathway.

7. 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.

8. These results show that, in MA-10 cells, the hLHR activates Fyn through an arrestin-3-dependent pathway and that this pathway is a mediator of the hLHR-provoked release of EGF-like growth factors.

Cow (Bovine) Arrestin 3, Retinal (X-Arrestin) (ARR3) interaction partners

1. Inositol hexakisphosphate (IP6) binds to the arrestin-3 phosphate sensor, and is stabilized by trimerization. Analysis of the trimerization surface, which is also the receptor-binding surface, suggests a feature called the finger loop as a key region of the activation sensor.

2. Several mutations in the two parts of the central "crest" of the arrestin molecule, middle-loop and C-loop, enhanced or reduced arrestin-3 interactions with several GPCRs in receptor subtype and functional state-specific manner.

3. K2A mutations in arrestin-1, -2, and -3 significantly reduced their binding to active phosphorhodopsin.

4. multiple residues on the non-receptor-binding side of arrestin-3 are crucial for JNK3 activation

5. Both nonvisual arrestin-2 and arrestin-3 are shown to directly bind Jun kinase (JNK)3alpha2 and its upstream activator Map kinase kinase (MKK)4; the affinity of arrestin-3 for these kinases is higher than that of arrestin-2.

6. the first crystal structure of arrestin-3, solved at 3.0 A resolution. Receptor binding.

7. SUMOylation sites in arrestin-3; arrestin-3 SUMOylation mediates beta(2)AR internalization

8. The nature of the changes in arrestin 3 distribution observed upon activation of adenosine receptors correlates with receptor sensitivity to G-protein-coupled receptor kinase-mediated phosphorylation and rapid internalization.

9. microtubule interaction may play a role in keeping p44 arrestin away from rhodopsin in dark-adapted photoreceptors