Ask about this productRelated genes to: ADORA2A antibody
- 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
Related products to: ADORA2A antibody
Related articles to: ADORA2A antibody
- 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 - : Dysregulation of purinergic signaling, particularly CD73 overexpression, influences tumor progression, immune evasion, and chemoresistance in hepatocellular carcinoma (HCC). We aimed to characterize the transcriptional landscape of this system, identify prognostic markers, and investigate how the tumor microenvironment modulates pharmacological response to combined sorafenib and doxazosin in 3D spheroid models. : We integrated RNA-seq data from The Cancer Genome Atlas-Liver Hepatocellular Carcinoma (TCGA-LIHC) to identify differentially expressed genes, pathway enrichment, gene co-expression networks, prognostic associations, and machine learning-based biomarker selection. Modulation of key targets was assessed in HepG2 and HepG2/LX-2 spheroids treated with sorafenib and doxazosin using qPCR and flow cytometry. : Transcriptomics revealed dysregulation and network fragmentation. Specifically, analysis of the TCGA cohort indicated that high expression of , , and correlated with poor overall survival. Given the critical role of CD73 in therapy resistance, we evaluated these findings in 3D models. Co-treatment significantly downregulated and mRNA expression, while was specifically reduced in the co-culture setting. For the , effect-size analysis revealed a large magnitude of inhibition in HepG2 spheroids. Although flow cytometry showed that high CD73 protein expression remained stable across treatments in co-culture, the combination therapy overcame stromal protection, significantly increasing apoptosis (active caspase-3) in both mono- and co-culture spheroids compared with vehicle and monotherapy. : We identified a purinergic prognostic signature in HCC and demonstrated that the combination therapy of sorafenib and doxazosin targets the adenosine pathway and specific receptors. We show that the stromal microenvironment sustains CD73 protein expression even under transcriptional inhibition, highlighting the critical role of 3D co-culture models in deciphering therapeutic resistance mechanisms. - Source: PubMed
Publication date: 2026/02/25
de Sousa Arieli CruzWeber Augusto FerreiraKlain ViníciusScholl Juliete NathaliRamos Jéssica Marques ObelarNascimento Natália Baltazar doGiehl Maria LuizaMartins Renata KrugerHeres João VitorDias Camila KehlMarschner RenataFigueiró FabrícioGuma Fátima Costa Rodrigues - Red microalga produces a sulfated exopolysaccharide (EPS), which enables its survival in challenging intertidal and spray zones. Extracellular polysaccharide hyaluronic acid (HA) plays important roles in skin hydration, elasticity, and volume. However, with aging, HA decreases and loses effectiveness, reducing skin moisture retention and firmness, and increasing signs of aging. An effective topical alternative to injectable HA replacement remains a largely unmet need. An extract of cultivated in natural sunlight, rich in EPS and polydeoxyribonucleotides (PDRNs), significantly activated the ADORA2A receptor in a CHO model, as well as reduced inflammation and increased collagen and HA production, autophagic flux, and key autophagy gene expression in dermal fibroblast cultures. In a double-blind clinical trial with placebo and HA benchmark controls, the extract delivered significant HA-like skin plumpness, hydration, and radiance benefits, and reduced signs of aging. The extract generally equaled or exceeded the HA benchmark. Its meaningful, swift HA-like activity shows potential for a safe, natural, and arguably more powerful HA-like alternative. - Source: PubMed
Publication date: 2026/03/01
Havas FabienKrispin ShlomoCohen MosheAttia-Vigneau Joan