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Validated All-in-One™ qPCR Primer for ADRA2C(NM_000683.3) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
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. The mouse studies 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 the alpha2C subtype, which contains no introns in either its coding or untranslated sequences.
Gene References into function
- Alpha2-ARs in vascular smooth muscle cells reflect differential activity of alpha2-AR gene promoters. Alpha2C-ARs can be induced via p38 MAPK-dependent pathway.
- Increased expression of alpha(2C)-adrenoceptors may contribute to enhanced cold-induced vasoconstriction and Raynaud's phenomenon.
- ADRA2C had one haplotype block of 10 kb
- alpha2CDel322-325 polymorphism is associated with increased sympathetic nervous and adrenomedullary hormonal activities, both during supine rest and during pharmacologically evoked catecholamine release
- A genetic variant of the alpha 2C-adrenoceptor subtype--resulting from the deletion of four consecutive amino acids at codons 322-325--confers a change in brain function playing a role in the pathogenesis of major depressive disorder.
- Genetic variations of the alpha and beta adrenergic receptors (alpha 2C Del322-325 allele) were found to be significant predictors of vasospastic angina
- Thus, the alpha(2C)AR alters alpha(2A)AR signaling by forming oligomers, and these complexes, which appear to be preferred over the homodimers, should be considered a functional signaling unit in cells in which both subtypes are expressed.
- alpha(2)-ARs might contribute neurotrophic actions in vivo synergistically or in permutation with other neurotrophic factors
- The ADRA2C deletion polymorphism had no effect on markers of resting sympathetic activity and cardiovascular measures, and did not account for ethnic differences in blood pressure.
- An estrogen-dependent increase in expression of cold-sensitive alpha(2C)-ARs may contribute to the increased activity of cold-induced vasoconstriction under estrogen-replete conditions
- Polymorphisms are not associated with Toureett's syndrome in this study.
- Because the alpha(2C)-adrenoceptor distribution pattern is conserved between rodents and humans, studies on the role of the alpha(2C)-adrenoceptor in rodent models of neuropsychiatric disorders may be relevant also for human diseases.
- Cyclic AMP acts through Rap1 and JNK signaling to increase expression of cutaneous smooth muscle alpha2C-adrenoceptors.
- Genetic variants in the alpha2C-adrenoceptor and G-protein contribute to ethnic differences in cardiovascular stress responses
- Genotype and haplotype of ADRA2C did not significantly affect survival in metoprolol-treated or carvedilol-treated heart failure patients.
- Beta1- and alpha2c-adrenoreceptor variants as predictors of clinical aspects of dilated cardiomyopathy in people of African ancestry.
- Our findings provide important evidence that the ADRA2C polymorphism is involved in the etiology of ADHD in Korean subjects.
- Three polymorphisms in ADRA2C and five polymorphisms in ADRB1 were involved in eight cross-validated epistatic interactions identifying several two-locus genotype classes with significant relative risks of death/transplant in heart failure patients
