Browse our Adrenergic, alpha-2C-, Receptor Proteins (ADRA2C)

Human Adrenergic, alpha-2C-, Receptor (ADRA2C) interaction partners

1. alpha2A- and alpha2C-adrenoceptors are functional receptors for norepinephrine, dopamine, and other previously assumed selective D2-like receptor ligands.

2. The frequency of alpha2CDel322-325-AR in suicide and non-suicide victims was similar. Genotype frequencies for the alpha2CDel322-325-AR polymorphism in depressed and schizophrenic subjects were higher than in controls, but these differences did not reach statistical significance. The results indicate that alpha2CDel322-325-AR may play a role in the pathophysiology of opiate abuse and dependence.

3. Immunoreactivity for ADRA2C was densely distributed in vascular smooth muscle of nasal turbinates.

4. ADRA2c is associated with heart rate recovery after exercise.

5. Common polymorphisms in the ADRA2C gene are not associated with orthostatic hypotension risk in Chinese.

6. Adrenergic receptor genotype influences heart failure severity and beta-blocker response in children with dilated cardiomyopathy.

7. alpha2C-adrenoreceptor interaction with filamin-2

8. Genetic variants of ADRA2C do not alter intracellular localization or plasma membrane trafficking.

9. the ADRA2C 322-325I/D genotype is a novel genetic risk marker for SBI among individuals with hyperhomocysteinemia.

10. the region comprising the N-terminal half of The receptors contributed to the alpha2C-selectivity of drug binding.

11. The ADRA2A and ADRA2C polymorphisms did not contribute to an increased risk of ischemic stroke or any pathophysiological subtype

12. Bucindolol prevents ventricular arrhythmias in subjects with heart failure and reduced left ventricular ejection fractions, and this effect is modulated by adrenergic alpha 2 receptor polymorphisms.

13. the predicted signal peptide in the N-terminal tail of the alpha(2C)-adrenoceptor does not act as a cleavable signal peptide

14. there is little evidence for an association between alpha(2C)Del322-325 polymorphism and an increased prevalence of left ventricular hypertrophy in patients with systemic hypertension.

15. alpha1b and alpha2c AR is over-expressed in basal-like breast tumours of poor prognosis

16. Genotype polymorphism frequencies for B1 receptor (amino acid positions 389 and 49) and alpha 2c receptor (deletion 322-325) are not significantly different in SC patients compared to female controls.

17. The alpha(2C)-Del322-325 polymorphism does not exhibit reduced signalling to adenylyl cyclase and may not represent a clinically important phenotype.

18. The common ADRA2C variant affected pain perception before and after dexmedetomidine but did not affect other cognitive responses

19. the norepinephrine lowering and clinical therapeutic responses to bucindolol were strongly influenced by alpha(2C) receptor genotype

20. 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.

Mouse (Murine) Adrenergic, alpha-2C-, Receptor (ADRA2C) interaction partners

1. Thyrotoxicosis depends on alpha2C-AR signaling to promote bone loss.

2. The sympathetic hyperactivity present in alpha2A/alpha2C-ARKO mice alters vascular reactivity only in certain types of arteries

3. alpha2A/alpha2C-adrenoceptor deletion accelerates cutaneous wound healing in mice

4. Expression of adrenergic alpha2C receptors is associated with peripheral involvement of antinociception induced by aerobic and resistance exercise.

5. In summary, our results highlight the importance of alpha(2R) distribution within the NTS regarding the neural control of blood pressure and the development of hypertension.

6. These findings suggest that beta(2)-AR is not the single adrenoceptor involved in bone turnover regulation and show that alpha(2)-AR signaling also may mediate the sympathetic nervous system actions in the skeleton.

7. Data indicate that alpha2C- and alpha1D- adrenoceptors interact to enhance adrenergic reactivity (norepinephrine-induced constriction) of mesenteric veins but not in mesenteric arteries.

8. adrenaline inhibits insulin release through alpha(2A)- and alpha(2C)-adrenergic receptors via distinct intracellular signaling pathways

9. alpha2C adrenoceptor expression is permissive under Adra2c-NN in central (cerebral cortex, hippocampus, subthalamus, hypothalamus, superior colliculus, cerebellum, and brain stem) and peripheral (pancreatic beta-islets) tissues

10. mRNAs encoding the alpha(2A)-adrenergic receptor are up-regulated in the brainstem.

11. Localized in the basal ganglia, alpha(2C)-adrenergic receptors are in a prime position to impact locomotor activity and are, therefore, potential targets of pharmacotherapy for ADHD.

12. Local cooling-induced reduction of skin blood flow in mice primarily results from increased reactivity of alpha (2C)-adrenoceptors to circulating catecholamines, in which the Rho/Rho kinase pathway is involved.

13. Exercise training decreased alpha(2A)/alpha(2C)adrenoceptor lacking mice's cardiac angiotensin II levels and angiotensin-converting enzyme activity.