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The current study demonstrated that a physiological concentration of adrenaline attenuates insulin (show INS Proteins) release via coupling of alpha2A-adrenoceptor to cAMP/TRPM2 (show TRPM2 Proteins) signaling.
This study showed that reduced expression of the alpha2A-adrenoceptor (Adra2a) which modulate antidepressant action in hippocampus.
Fzd5 and Trvp6 are expressed in the epithelial layer of the prospective pyroric and glandular stomach, respectively and Adra2a is expressed in the mesenchymal region of the stomach primordium at the beginning of morphogenesis.
The sympathetic hyperactivity present in alpha2A/alpha2C-ARKO (show CYP19A1 Proteins) mice alters vascular reactivity only in certain types of arteries
Data indicate that activation of alpha(2A) adrenergic receptor (alpha(2A)AR) signaling disrupts transgenic amyloid precursor protein (APP (show APP Proteins)) interaction with sorting-related receptor with A repeat (SorLA (show SORL1 Proteins)) in cells and brain.
Thus, our study reveals distinct actions of PBN afferents within the BNST and suggests that alpha(2A)-AR agonists may filter excitatory transmission in the BNST by inhibiting a component of the PBN input while enhancing the actions of other inputs.
The time course of Adra2a- and dopamine D2R (show DRD2 Proteins)-mediated transmission reflects underlying differences in the extent of spillover and pooling of inhibitory postsynaptic potentials (IPSPs).
Activation of alpha2A-AR and muscarinic M3 receptors affects the initial [Ca(2 (show CA2 Proteins)+)] response to increase of glucose from 3 to 20mM in BETA-cells.
Canonical betaAR-mediated signaling coupled to PKA activation results in phosphorylation of spinophilin (show PPP1R9B Proteins), disrupting its interaction with alpha2AARs and accelerating alpha2AAR endocytic responses.
conformational change of alpha(2A)AR by voltage is independent from receptor-G protein docking and regulates receptor signaling, including beta-arrestin binding, activation of G proteins, and G protein-activated inwardly rectifying K(+) currents
ADRA2A genetic variation contributes independently to the risk of GDM in Caucasian women.
Results describe association of ADRA2A rs553668 with type 2 diabetes in a Mexican population.
Significant group*genotype interactions were found for 3 ADRA2A variants revealing steeper delay discounting (DD) in cocaine users (but not controls) carrying the G-allele of rs1800544, the T-allele of rs521674 and the C-allele of rs602618. High ADRA2A mRNA expression levels were significantly associated with a reduced tendency to choose smaller more immediate rewards in cocaine users.
The summary of this study, none of the examined variants reached the threshold for statistical significance after correction for multiple testing. The SNP rs1800544 in ADRA2A, revealed nominally significant association, but the direction of effect was the opposite to that reported in previous studies conducted in children and adolescents.
The results of this study suggested that ADRA2A rs3750625 contributes to poststress musculoskeletal pain severity by modulating miR (show MLXIP Proteins)-34a regulation
This study reveled that ADA2A are up regulate in peripheral blood mononuclear cells in patient with multiple sclerosis.
Results show that ADRA2A genetic variants are associated with blood glucose and stress-induced hyperglycemia after acute myocardial infarction in Caucasians.
These findings suggest that Gi1 interacts only with active GPCRs and that the well known high speed of GPCR signal transduction does not require preassembly between G proteins and GPCRs.
ADRA2A Germline Gene Polymorphism is Associated to the Severity, but not to the Risk, of Breast Cancer.
Risk alleles for 6 loci increased glucose levels from birth to 5 years of age (ADCY5 (show ADCY5 Proteins), ADRA2A, CDKAL1 (show CDKAL1 Proteins), CDKN2A/B, GRB10 (show GRB10 Proteins), and TCF7L2 (show TCF7L2 Proteins)
islets express mRNA transcripts for sulfonylurea receptor 1 (Sur1 (show ABCC8 Proteins)), inward rectifying potassium channel (show KCNAB2 Proteins) (Kir6.2 (show KCNJ11 Proteins), associated with Sur1 (show ABCC8 Proteins)), glucagon-like peptide 1 receptor (GLP1R (show GLP1R Proteins)), and adrenergic receptor alpha 2A (ADRalpha2A)
Proliferation of Achilles tenocytes in overuse tendinosis is induced by ADRA2A stimulation and inhibited by an ADRA2A blocker.
Alpha-2-adrenergic receptors are members of the G protein-coupled receptor superfamily. They include 3 highly homologous subtypes: alpha2A, alpha2B, and alpha2C. These receptors have a critical role in regulating neurotransmitter release from sympathetic nerves and from adrenergic neurons in the central nervous system. Studies in mouse revealed that both the alpha2A and alpha2C subtypes were required for normal presynaptic control of transmitter release from sympathetic nerves in the heart and from central noradrenergic neurons\; the alpha2A subtype inhibited transmitter release at high stimulation frequencies, whereas the alpha2C subtype modulated neurotransmission at lower levels of nerve activity. This gene encodes alpha2A subtype and it contains no introns in either its coding or untranslated sequences.
, alpha-2A adrenergic receptor
, alpha-2A adrenoceptor
, alpha-2A adrenoreceptor
, alpha2A-adrenergic receptor
, adrenergic receptor subtype alpha-2A
, adrenergic, alpha-2A-, receptor
, alpha-2A-adrenergic receptor
, adrenergic receptor alpha-2A
, alpha-2A adrenergic receptor-like
, subtype alpha2-C10
, adrenergic alpha 2A, receptor
, adrenergic, alpha-2, receptor
, alpha-2-adrenergic receptor
, alpha-2D adrenergic receptor
, alpha-2 adrenergic receptor subtype C10
, alpha-2-adrenergic receptor, platelet type
, alpha-2AAR subtype C10
, adrenergic receptor, alpha 2a
, alpha 2A adrenoceptor