-
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.
-
These studies suggest a previously unrecognized and novel role for GRK6 in neutrophil migration specific to pulmonary tissue during bacterial infection.
-
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.
-
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.
-
GRK6-mediated OXTR desensitization in labor is necessary for normal uterine contractile patterns and optimal fetal outcome.
-
It regulates apoptotic engulfment in phagocytes. (review)
-
GRK6 directly phosphorylates Nfkbia at Ser32/Ser36. Knockdown of GRK6 suppresses TNF-alpha-induced NF-kappaappaB signaling.
-
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.
-
data demonstrate that GRK6 plays a feedback regulatory role in CXCR2-mediated tumor development, invasion and metastasis
-
G-protein-coupled receptor kinase 6 (GRK6) is involved in apoptotic cell clearance.
-
Chemokine receptor CXCR2 interacts with GRK6 to negatively regulate receptor sensitization and trafficking, thus affecting cell signaling and angiogenesis.
-
Results identify GRK5/6 as novel kinases for the single transmembrane receptor LRP6 during Wnt signaling.
-
deficiency causes defective lymphocyte chemotaxis
-
Postsynaptic D2-like dopamine receptors are physiological targets for GRK6 and suggests that this regulatory mechanism contributes to central dopaminergic supersensitivity.
-
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.
-
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.
-
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.
-
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.
-
Data show an important protective role for GRK6 against post-inflammatory visceral hyperalgesia.
-
these results suggest that GRK6 may play a role in regulating some, but not all morphine-mediated responses.
