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Human Polyclonal ADRBK2 Primary Antibody pour EIA, IHC (p) - ABIN950649
Rao, Rapoport, Kim: Decreased GRK3 but not GRK2 expression in frontal cortex from bipolar disorder patients. dans The international journal of neuropsychopharmacology / official scientific journal of the Collegium Internationale Neuropsychopharmacologicum (CINP) 2009
Show all 2 Pubmed References
GRK3 controls cardiac alpha1-adrenergic receptor responsiveness
Study found that GRK3 was significantly overexpressed in 162 pairs of colon cancer tissues than in the matched noncancerous mucosa. These data show that aberrant expression of GRK3 plays an important role in promoting colon cancer progression through enhanced proliferation and reduced apoptosis.
hat expression of GRK3 was down-regulated in pancreatic ductal adenocarcinoma and was an independent prognostic factor
GRK3 is a new critical activator of neuroendocrine phenotypes and mediator of CREB activation in promoting neuroendocrine differentiation of prostate cancer cells.
effects of GRK3 modulation appear to be specific to chemokine-mediated migration behaviors without influencing tumor cell proliferation or survival
data are consistent with the possibility that oncogenes can induce cellular stiffness via an HDAC6-induced reorganization of the vimentin intermediate filament network
Data indicate that CXCL12-induced phosphorylation at CXCR4 S346/347 was mediated by GRK2/3.
In oral squamous cell carcinomas, malignant cells and surrounding tissue overexpress the ADRBK2 gene.
A reduced cortical concentration of GRK3 in schizophrenia (resembling that in aging) may result in altered G protein-dependent signaling, thus contributing to prefrontal deficits in schizophrenia.
GRK3 is a negative regulator of cell growth whose expression is preferentially reduced in glioblastoma of the classical subtype as a consequence of activity in primary gliomagenic pathways.
mRNA levels for GRK3 were inversely correlated with systolic and diastolic blood pressure (day, night and 24 h), which suggests a protective role for GRK3 in the regulation of human blood pressure
we found no evidence of altered levels of acetylated histone H3 at the affected allele compared to the common allele
dysregulation in GRK3 expression alters signaling desensitization, and thereby predisposes to the development of bipolar disorder
the CRH-R1alpha carboxyl tail is important for regulation of receptor activity by G protein-coupled receptor kinase
ATP stimulation leads to GRK3 phosphorylation of P2X(7) receptor.
No support for a major role for GRK3 gene promoter variants in cocaine addiction.
Dysregulation in GRK3 expression alters signaling desensitization and thereby predisposes to the development of bipolar disease.
role for GRK3 in regulating CXCR4 attenuation and have provided a mechanistic link between the GRK3 pathway and the CXCR4-related WHIM(WT) disorder.
The G-384A variant may alter binding of Sp1/Sp4 transcription factors resulting in an increase in gene transcription and an increase in vulnerability to bipolar disorder.
beta-arrestin 2 and GRK2 colocalize with S1p2 in developing zebrafish embryos and depletion of GRK2 in the S1p2 R150H miles apart zebrafish partially rescued cardia bifida.
GRK2 and GRK5 control cardiac function as well as morphogenesis during development although with different morphological outcomes.
Data suggest that a G protein-coupled receptor kinase, perhaps GRK2 or 3, functions as a vertebrate kinase for Smoothened, promoting Hedgehog signal transduction during early development.
These data thus reveal a novel kinase activity-independent function for GRK and establish a role for GRK2 as a cell-cycle regulator during early embryonic development.
Fusion proteins containing the c-terminus of GPCR kinase 3 (GRK3ct) and either the fluorescent protein cerulean or Renilla luciferase bind to venus-labeled Gbetagamma dimers, resulting in Forster or bioluminescence resonance energy transfer.
The beta-adrenergic receptor kinase specifically phosphorylates the agonist-occupied form of the beta-adrenergic and related G protein-coupled receptors. Overall, the beta adrenergic receptor kinase 2 has 85% amino acid similarity with beta adrenergic receptor kinase 1, with the protein kinase catalytic domain having 95% similarity. These data suggest the existence of a family of receptor kinases which may serve broadly to regulate receptor function.
adrenergic, beta, receptor kinase 2
, beta-adrenergic receptor kinase 2-like
, beta ARK2
, beta-adrenergic receptor kinase 2
, G-protein-coupled receptor kinase 3
, adrenergic receptor kinase, beta 2 (G-protein-linked receptor kinase)
, G-protein coupled receptor kinase 2/3