Browse our anti-G Protein-Coupled Receptor Kinase 6 (GRK6) Antibodies

Human G Protein-Coupled Receptor Kinase 6 (GRK6) interaction partners

1. GRK6 overexpression can significantly enhance tumor proliferation and invasion, which was consistent with clinical findings.

2. demonstrate for the first time exosomal enrichment of G-protein-coupled receptor kinase (GRK) 5 and GRK6, both of which regulate Src and IGF-IR signaling and have been implicated in cancer.

3. Genetic variation in OXTR and GRK6 is associated with the amount of oxytocin required as well as the duration of labor and risk for cesarean delivery among women undergoing induction of labor near term.

4. This work demonstrates the importance of GRK6 in regulation of hematopoietic stem cell self-renewal and reveals its potential role in participation of stress response.

5. Decreased expression of GRK6 may serve as an independent predictor of overall survival in lung adenocarcinoma.

6. The expression of GRK6 mRNA and protein was significantly lower in hypopharyngeal squamous cell carcinoma than in corresponding adjacent non-tumor tissues. This was associated with aberrant methylation of the gene.

7. Our results imply that GRK6 may not play a role in the pathophysiology of schizophrenia among Han Chinese

8. these results indicate that GRK6 complexes with AGS3-Galphai2 to regulate CXCR2-mediated leukocyte functions at different levels, including downstream effector activation, receptor trafficking, and expression at the cell membrane.

9. GRK6 plays a predominant role in phosphorylation of FFA receptor (FFA)4.

10. results suggested that GRK6 overexpression plays an important role in hepatocellular carcinoma

11. Downregulation of GRK6 expression enhances CXCR4 signaling and promoted medulloblastoma cell migration.

12. A reduced cortical concentration of GRK6 in schizophrenia (resembling that in aging) may result in altered G protein-dependent signaling, thus contributing to prefrontal deficits in schizophrenia.

13. inhibition of GRK6 represents a uniquely targeted novel therapeutic strategy in human multiple myeloma.

14. A number of double mutations of GRK6 kinase within helices 3, 9, and 10 reduced phosphorylation of the beta2 adrenergic receptor and rhodopsin compared to wild-type GRK6 kinase.

15. Recruitment of beta-Arrestin 2, but not beta-Arrestin 1, to the active WHIM-mutant receptor is delayed compared to the WT CXCR4 receptor and Grk6 fails to associate with the WHIM-mutant receptor.

16. Results identify GRK5/6 as novel kinases for the single transmembrane receptor LRP6 during Wnt signaling.

17. potential role of endogenous GRK6 in the regulation of M(3) mACh receptor

18. GRK6 is potential marker for organ injury and survival after cardiopulmonary bypass

19. the CRH-R1alpha carboxyl tail is important for regulation of receptor activity by G protein-coupled receptor kinase

20. the crystalline GRK6 RGS homology domain forms an extensive dimer interface using conserved hydrophobic residues distinct from those in GRK2 that bind Galpha(q)

Mouse (Murine) G Protein-Coupled Receptor Kinase 6 (GRK6) interaction partners

1. These data indicate that GRK2, GRK5 and GRK6 redundantly modulate Smo-GATA crosstalk in fetal mouse hearts, orchestrating transcriptional pathways previously linked to clinical and experimental atrioventricular canal defects

2. findings show that chemerin-activated CMKLR1 regulation in inflammatory macrophages is largely GRK6 and beta-arrestin mediated, which may impact innate immunity and have therapeutic implications in rheumatic disease.

3. Conditions for optimal dendritic cells guidance are perfectly provided by the CCL21 gradients measured in vivo. Furthermore, CCR7 signal termination by the G-protein-coupled receptor kinase 6 (GRK6) is crucial for haptotactic but dispensable for chemotactic CCL21 gradient sensing in vitro and confirm those observations in vivo.

4. These studies suggest a previously unrecognized and novel role for GRK6 in neutrophil migration specific to pulmonary tissue during bacterial infection.

5. Silencing of GRK6 expression by siRNA impairs CXCR4-serine 339 phosphorylation and migration of cardiac stem cellss caused by SCF. In vivo, knockdown of GRK6 impairs the ability of CSCs to migrate into peri-infarcted areas.

6. This work demonstrates the importance of GRK6 in regulation of hematopoietic stem cell self-renewal and reveals its potential role in participation of stress response.

7. GRK6-mediated OXTR desensitization in labor is necessary for normal uterine contractile patterns and optimal fetal outcome.

8. It regulates apoptotic engulfment in phagocytes. (review)

9. GRK6 directly phosphorylates Nfkbia at Ser32/Ser36. Knockdown of GRK6 suppresses TNF-alpha-induced NF-kappaappaB signaling.

10. these results indicate that GRK6 complexes with AGS3-Galphai2 to regulate CXCR2-mediated leukocyte functions at different levels, including downstream effector activation, receptor trafficking, and expression at the cell membrane.

11. data demonstrate that GRK6 plays a feedback regulatory role in CXCR2-mediated tumor development, invasion and metastasis

12. G-protein-coupled receptor kinase 6 (GRK6) is involved in apoptotic cell clearance.

13. Chemokine receptor CXCR2 interacts with GRK6 to negatively regulate receptor sensitization and trafficking, thus affecting cell signaling and angiogenesis.

14. Results identify GRK5/6 as novel kinases for the single transmembrane receptor LRP6 during Wnt signaling.

15. deficiency causes defective lymphocyte chemotaxis

16. Postsynaptic D2-like dopamine receptors are physiological targets for GRK6 and suggests that this regulatory mechanism contributes to central dopaminergic supersensitivity.

17. In the absence of GRK6, the G-CSF-induced increase in circulating neutrophils is profoundly impaired. After injection of pegylated-G-CSF, significantly lower numbers of circulating neutrophils were observed in GRK6-/- as compared with wild-type (WT) mice.

18. The results suggest that mouse G-protein-coupled receptor kinase isoform 6-C may be considered a basic, prototypic representative of the GRK4-like kinases.

19. 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.

20. GRK6 and -2, but not GRK5, are involved in the pathogenesis of acute arthritis in the K/BxN model. In particular, GRK6 may dampen inflammatory responses by regulating granulocyte trafficking toward chemoattractants.