ADORA2a ELISA kit
- Known as:
- ADORA2a Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ADORA2a-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ADORA2a ELISA kit
Related genes to: ADORA2a ELISA kit
- Gene:
- ADORA2A NIH gene
- Name:
- adenosine A2a receptor
- Previous symbol:
- ADORA2
- Synonyms:
- RDC8
- Chromosome:
- 22q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1991-03-11
- Date modifiied:
- 2014-11-19
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- The global impact of pulmonary tuberculosis (PTB) is compounded by a limited understanding of modifiable risk factors. While caffeine is the most consumed psychoactive substance, its causal relationship with PTB and the underlying immunological mechanisms remain unknown. - Source: PubMed
Publication date: 2026/04/20
Zhu LiangyuZheng ZidaHuang XunLu HaoranChen ZhiqiangWu HanxinPeng LiTao LvyanBai YueYang RuiBao RuianLuo SuyiMa WeijiangSong JieqinTang JiaomeiLi BingxueBao FukaiLiu Aihua - Caffeine is the most widely consumed psychoactive stimulant worldwide and acts primarily through antagonism of adenosine A1 and A2A receptors, thereby reducing sleep pressure and promoting wakefulness. Although its alerting and performance-enhancing effects are well established, its influence on sleep-related electroencephalography (EEG) has been investigated across diverse paradigms with substantial methodological heterogeneity. This systematic and mechanistic review aimed to synthesize human evidence on how caffeine affects sleep architecture, quantitative sleep EEG, and neurophysiological markers of sleep homeostasis, and to interpret these findings within current models of adenosine-mediated sleep-wake regulation. - Source: PubMed
Publication date: 2026/04/13
Chmiel JamesKurpas Donata - L-DOPA-induced dyskinesia is attributed to opposite activity changes mediated by D1 and D2 dopamine receptors in the two striatal output pathways. Whereas the causal role of direct-pathway D1 receptors is well established, the specific involvement of indirect-pathway D2 receptors in dopaminergic dyskinesias has remained elusive. - Source: PubMed
Publication date: 2026/04/20
Andreoli LauraNyman TeodorEspa ElenaJakobsson JohanElabi Osama FCenci Maria Angela - Cutaneous leishmaniasis (CL) caused by Leishmania braziliensis is characterized by intense inflammation that contributes both to parasite control and tissue pathology. Purinergic signalling, particularly mediated by adenosine and its receptors, has been implicated in immune modulation during Leishmania infection, yet its functional relevance in L. braziliensis remains poorly defined. Here, we investigated the roles of adenosine A2A and A2B receptors and adenosine deaminase (ADA) in regulating immune responses during L. braziliensis infection. Transcriptomic analyses of human CL lesions revealed increased expression of ADORA2A, which paradoxically correlated positively with pro-inflammatory and microbicidal gene signatures. Despite modulating the receptor expression on L. braziliensis-infected macrophages as well, pharmacological inhibition of A2A or A2B receptors did not affect parasite burden, reactive oxygen species (ROS) production, or inflammatory cytokine release. Thus suggesting that adenosine receptor signalling is dispensable in this context. In contrast, ADA and ADA2 were markedly upregulated in CL lesions and infected macrophages and showed strong positive correlations with inflammatory mediators. Functional inhibition of ADA with pentostatin significantly increased intracellular parasite load and reduced ROS, TNF-α, and IL-1β production, demonstrating a critical role for ADA in sustaining macrophage microbicidal activity. These findings suggest that ADA activity is central to modulating adenosine-mediated immunosuppression in CL and may serve as both a biomarker of disease activity and a potential therapeutic target. - Source: PubMed
Publication date: 2026/04/18
de Paula Wesley Limade Oliveira Geovanna MedeirosRibeiro-Dias FátimaGomes Rodrigo Saar - Therapeutic responsiveness in urologic cancers is gated by metabolic-immune coupling that conditions tumor-associated macrophages (TAMs). Myeloid-dominated "cold" ecosystems blunt antigen handling, phagocytosis, and trafficking, limiting the benefit of immune-checkpoint inhibitors (ICIs). This review focuses on three high-value axes that shape TAM state and niche: the lactate-pH / hypoxia-HIF-VEGF axis that enforces acidic, adenosinergic suppression and angiogenic programs; lipid rafts axis that stabilizes inhibitory hubs (e.g., PI3K-AKT/TREM2) and skews phagocytosis/antigen presentation; and ferroptosis-redox axis control that sets inflammatory versus tolerogenic set-points. The review further outlines pharmacodynamic anchors-hyperpolarized C-pyruvate MRI (k), soluble ANGPT2, and spatial NT5E/ADORA2A modules-to operationalize a bench-to-biomarker-to-bedside loop using organoid-immune co-cultures, humanized/xenograft systems, and tumor slices. This framework prioritizes adaptive enrichment for glycolysis- or adenosine-high tumors, rational timing/sequencing with ICIs, and avoidance of global myelosuppression. Collectively, metabolism-informed TAM re-education offers a route to convert myeloid-dominated "cold" ecosystems into treatment-responsive states across urologic cancers. - Source: PubMed
Publication date: 2026/02/26
Huang WenxueLi WeijiaShangguan WentaiYang LinLi ZhuohangSun BoyuanMa CunzhenYang XunguoPeng PeidanZhao JieCheng BishengWu Peng