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Validated All-in-One™ qPCR Primer for ADORA2B(NM_000676.2) 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
This gene encodes an adenosine receptor that is a member of the G protein-coupled receptor superfamily. This integral membrane protein stimulates adenylate cyclase activity in the presence of adenosine. This protein also interacts with netrin-1, which is involved in axon elongation. The gene is located near the Smith-Magenis syndrome region on chromosome 17. [provided by RefSeq].
Gene References into function
- 1,8-disubstituted xanthine derivatives: synthesis of potent A2B-selective adenosine receptor antagonists
- A2BR binds to E3KARP and Ezrin upon agonist stimulation.
- Mast cell-mediated stimulation of angiogenesis: cooperative interaction between A2B and A3 adenosine receptors.
- Selectively up-regulated by hypoxia (>5-fold increase in mRNA), and antagonists neutralize ATP-mediated endothelial permeability
- demonstrated induction of IgE synthesis by the interaction between adenosine-stimulated mast cells and B lymphocytes involves up-regulation of IL-4 and IL-13 mediated by A(2B) receptors
- Interferon-gamma down-regulates adenosine 2b receptor-mediated signaling and inhibits the expression of adenylate cyclase
- adenosine A2B receptors mediate the adenosine-induced contraction vasomotor effect in human chorionic vessels and that this involves synthesis of a thromboxane receptor activator or a related prostanoid.
- The PKC delta and epsilon isoforms are also involved in adenosine receptor A(2b) dependent upregulation of IL-6 expression.
- A(2B) receptors may play role in regulating glomerular remodeling associated with glomerular mesangial cell proliferation. Activation of A(2B) receptors may prevent glomerular remodeling associated with renal disease, hypertension, and diabetes.
- A2bR signals through adenylate cyclase (AC) 6 isoform in intestinal epithelial cells
- A(2B) receptors up-regulate IL-4 through G(q) signaling that is potentiated via cross-talk with G(s)-coupled pathways.
- Data indicate that adenosine increases the release of IL-19 from bronchial epithelial cells via activation of adenosine A(2B) receptors, and IL-19 in turn activates human monocytes to release TNF-alpha, which upregulates A(2B) receptor expression.
- Transcriptional coordination of adenosine a2B receptor by HIF-1alpha and amplified adenosine signaling during hypoxia.
- adenosine treatment of dermal papilla cells upregulates FGF-7 expression via the A2b adenosine receptor and that cAMP acts as one of the second messengers in this pathway
- Adenosine is not a direct GHSR agonist. In human embryonic kidney 293s (HEK) cells expressing GHSR, adenosine activates endogenously expressed A(2B)R resulting in calcium mobilization.
- Epac1 activation in HUVEC results in ERK1/2 activation, and this protein, at least in part, mediates response to the physiologically relevant event of A(2B)AR stimulation
- Short-term TNF-alpha cell treatment caused A(2B) AR phosphorylation inducing, in turn, impairment in A(2B) AR-G protein coupling and cAMP production
- Pharmacologic and genetic evidence for vascular A2BAR signaling as central control point of hypoxia-associated vascular leak.
- The results herein provide initial evidence that the inhibitory effect of hypoxia on MMP-9 by mature dendritic cells requires the activation of A(2b) in a cAMP/PKA-dependent pathway.
- our findings revealed the role of adenosine receptors in breast cancer cell lines on growth modulation role of A3 and functional form of A2B, although its involvement in cell growth modulation was not seen
- A(2B)-R are required for ASL volume homeostasis in human airways, and therapies directed at inhibiting A(2B)-R may lead to a cystic fibrosis-like phenotype with depleted ASL volume and mucus stasis.
- A2B adenosine receptors may differentially modulate hENTs in hPMEC, which could be a mechanism attempting to re-establish physiological extracellular adenosine levels in pre-eclampsia.
