ADRA2A
- Known as:
- ADRA2A
- Catalog number:
- 001241A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADRA2A
Related genes to: ADRA2A
- Gene:
- ADRA2A NIH gene
- Name:
- adrenoceptor alpha 2A
- Previous symbol:
- ADRA2, ADRA2R
- Synonyms:
- ADRAR
- Chromosome:
- 10q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2019-03-22
Related products to: ADRA2A
Related articles to: ADRA2A
- It's been reported that illicit drug supplies increasingly contain the α -adrenergic agonist, xylazine, alongside fentanyl, yet the pharmacological basis for the greater lethality of this combination remains unclear. Prior research has shown that μ-opioid (Oprm1) receptors, on which fentanyl acts, and α -adrenergic (Adra2a) receptors, on which xylazine acts, are both expressed within brainstem circuits that govern autonomic control, especially the parabrachial (PB) and Kölliker-Fuse (KF) nuclei that regulate respiration. Thus, we propose that co-activation of these inhibitory receptors and their respective pathways could potentiate or additively suppress respiratory and thermoregulatory function. - Source: PubMed
Publication date: 2026/04/24
Lynch NicoleLima Janayna DBandaru SathyajitMachado NataliaKaur Satvinder - The nervous system drives tumor growth directly through intra-tumoral axons and indirectly through the systemic action of hormones. Yet contexts where the nervous system inhibits tumor growth are less defined. Here, we performed optical reconstruction of axonal innervation in mouse models of cutaneous melanoma, revealing progressive innervation by sympathetic axons. Local depletion of these axons accelerates while local optogenetic activation slows melanoma growth, together consistent with these axons acting as a physiological growth brake. The sympathetic nervous system is typically associated with driving tumor growth through activation of β-adrenergic receptors (ARs). Here, we find that the initial tumor seeding conditions sensitize melanomas from βAR-driven growth promotion toward α2-AR-driven growth inhibition. Mechanistically, the axonal activation of α2 ARs restricts the number and distribution of pro-tumor myeloid cells, independently of T cell activity. Together, our data reveal context-dependent, bidirectional neural control of tumor progression. - Source: PubMed
Publication date: 2026/04/29
Liu TingtingKutsovsky Daniel YEarlie Ethan MJi LiangliangIskols MichaelRamsamooj ShaktiDawkins Xavier IZerhouni MarwaBirbrair AlexanderPiskounova ElenaLi Ming OLaughney Ashley MSimon David J - Here, we create a conditional line and use it to show that sedative, hypnotic, and hypothermic effects of α -agonists are neuronally mediated via the α adrenergic receptor. - Source: PubMed
Publication date: 2026/04/17
Fryou Noah LJiang TimothyFrick NathanKwasniewska PaulaLipin Mikhail YKelz Max BThomas Steven AMcKinstry-Wu Andrew - Stress is known to play a critical role in relapse to drug use as well as in food craving. Craving itself is a key determinant of relapse, and cue-induced drug craving has been shown to increase, or 'incubate', over time for certain drugs such as cocaine and nicotine, though this effect is less consistent for others such as opiates. However, the modulations of stress-related biochemical systems after early or protracted withdrawal that could contribute to this incubation phenomenon have not yet been systematically examined in animal models, nor has the specificity of these mechanisms been tested across different drug classes or reinforcers. To address this gap, we analysed brains from male Lewis rats that self-administered cocaine (0.75 mg/kg, i.v.), heroin (0.075 mg/kg, i.v.), or saline, and subsequently assessed changes in plasma corticosterone, ornithine and other stress-related amines, alongside central gene and protein expression CRH, CRH2 receptor, and α- and β-adrenergic receptor subunits -Adra1, Adra2a and Adrb1) in cortico-striato-amygdalar nodes (after 1 or 30 days of withdrawal). A parallel experiment was conducted using sucrose as a reinforcer. Our findings indicate that although most effects were reinforcer-specific, convergent adaptations were also observed, particularly within noradrenergic systems and the basolateral amygdala, expanding our knowledge about the neurochemical rearrangements occurring during withdrawal. - Source: PubMed
Publication date: 2026/04/16
Roura-Martínez DavidUcha MarcosMoreno-Fernández MarioCastillo Carlos AlbertoBallesteros-Yáñez InmaculadaMarcos AlbertoAmbrosio EmilioHiguera-Matas Alejandro - Raynaud's phenomenon (RP) is the first noticeable symptom of systemic sclerosis (SSc), appearing even years before other signs. Vascular and immune pathways, hallmarks in SSc pathogenesis, are implicated in primary RP. Hence, we aimed to define the shared genetic architecture between these conditions to explore pathogenic mechanisms and whether pleiotropic loci could help identify primary RP patients at increased genetic risk of developing SSc. - Source: PubMed
Publication date: 2026/04/08
Rangel-Peláez CarlosRodriguez-Martin InmaculadaRosa-Baez CarlosKerick MartinDel-Castillo Alfredo Guillen-Simeón-Aznar Carmen PCallejas José LDistler OliverProudman Susanna MNikpour MandanaHunzelmann NicolasMoroncini Gianlucade Vries-Bouwstra Jeska KHerrick Ariane LAllanore YannickAlarcón-Riquelme Marta EBeretta LorenzoMayes Maureen DDenton Christopher PAssassi ShervinMartín JavierAcosta-Herrera MarialbertOrtiz-Fernández Lourdes