Anti-Human Adenosine A2a R monoclonal antibody (CABT-L3037)

Mouse Anti-Human Adenosine A2a R monoclonal antibody for ELISA, FC

Specifications


Host Species
Mouse
Antibody Isotype
IgG2a
Clone
600828
Species Reactivity
Human
Immunogen
NS0 mouse myeloma cell line transfected with human Adenosine A2a R (AA Met1-Ser412)
Conjugate
Unconjugated

Target


Alternative Names
ADORA2A; adenosine A2a receptor; A2aR; RDC8; ADORA2; adenosine receptor A2a
Entrez Gene ID

Citations


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References


Acute effects of caffeine on attention: a comparison of non-consumers and withdrawn consumers

JOURNAL OF PSYCHOPHARMACOLOGY

Authors: Smith, Andrew P.; Christopher, Gary; Sutherland, David

Despite the large number of studies on caffeine and attention, interpretation is often difficult because of methodological weaknesses. In the present study, use of a small battery of tests with four key outcome measures, combined with an appropriate sample size, addresses many of these problems. This methodology was used to examine whether effects of caffeine (a dose of 2 mg/kg) could be explained in terms of reversal of the effects of caffeine withdrawal. This was achieved by examining effects in non-consumers (N = 35), who could not be withdrawn, and also in a group of consumers (N = 35) who had undergone withdrawal for a week and no longer reported symptoms of withdrawal. The results showed no effect of short-term withdrawal on the performance measures, even though subjective reports showed an increase in symptoms after withdrawal. In contrast, the caffeine challenge carried out on Day 8 showed that ingestion of caffeine was associated with faster simple reaction time, fewer long responses, greater detection of targets in the cognitive vigilance task, and faster encoding of new information. These results suggest that it is important to continue to investigate mechanisms underlying these effects of caffeine and to further evaluate the practical implications of such effects.

Increased striatal adenosine A(2A) receptor levels is an early event in Parkinson's disease-related pathology and it is potentially regulated by miR-34b

NEUROBIOLOGY OF DISEASE

Authors: Villar-Menendez, Izaskun; Porta, Silvia; Buira, Sandra P.; Pereira-Veiga, Thais; Diaz-Sanchez, Sara; Luis Albasanz, Jose; Ferrer, Isidre; Martin, Mairena; Barrachina, Marta

Adenosine A(2A) receptor (A(2A)R) is a G-protein coupled receptor that stimulates adenylyl cyclase activity. In the brain, A(2A)Rs are found highly enriched in striatal GABAergic medium spiny neurons, related to the control of voluntary movement. Pharmacological modulation of A(2A)Rs is particularly useful in Parkinson's disease (PD) due to their property of antagonizing dopamine D-2 receptor activity. Increases in A(2A)R levels have been described in PD patients showing an important loss of dopaminergic denervation markers, but no data have been reported about A(2A)R levels in incidental PD brains. In the present report, we show that increased A(2A)Rs protein levels were also detected in the putamen of incidental PD cases (Braak PD stages 1-2) with respect to age-matched controls. By contrast, A(2A)Rs mRNA levels remained unchanged, suggesting that posttranslational mechanisms could be involved in the regulation of A(2A)Rs. It has been described how miR-34b/c downregulation is an early event in PD cases. We found that miR-34b levels are also significantly reduced in the putamen of incidental PD cases and along disease progression. Given that 3'UTR of A(2A)R contains a predicted target site for miR-34b, the potential role of this miRNA in protein A(2A)R levels was assessed. In vitro studies revealed that endogenous A(2A)R protein levels increased when miR-34b function was blocked using a specific anti-miR-34b. Moreover, using a luciferase reporter assay with point mutations in a miR-34b predicted binding site within the 3'UTR region of A(2A)R mRNA abolished the effect of the miRNA using a miR-34b mimic. In addition, we showed a reduced percentage of DNA methylation in the 5'UTR region of ADORA2A in advanced PD cases. Overall, these findings reveal that increased A(2A)R protein levels occur in asymptomatic PD patients and provide new insights into the molecular mechanisms underlying A(2A)R expression levels along the progression of this neurodegenerative disease. (C) 2014 Elsevier Inc. All rights reserved.

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