-
Hypothalamic expression of A1R, are increased in the diet-induced obesity mouse model.
-
Loss of A1AR expression results in an increased susceptibility to noise-induced cochlear neural injury and hearing loss.
-
Expression of the SENP2 gene was suppressed by theobromine. In vivo knockdown studies showed that AR1 knockdown in mice attenuated the anti-adipogenic effects of theobromine in younger mice. Theobromine suppresses adipocyte differentiation and induced C/EBPbeta degradation by increasing its sumoylation.
-
The three receptor sets considered (mAChR, AR and TrkB receptors) intervene in modulating the conditions of the competition between nerve endings.
-
Systemic inflammatory response syndrome-associated lymphopenia is initiated by A1R desensitization and adenosine-mediated inhibition of IL-15 production is part of the mechanism that accounts for the delay in leukopenia recovery in patients with severe sepsis.
-
Results demonstrated a significant downregulation of adenosine A1 receptors in the cortex and striatum, concomitant to striatal D2R downregulation in iron deficient mice and rats.
-
Adenosine A1A receptor and adenosine A3A receptor agonists and adenosine 5'-monophosphate cause regulated hypothermia that was characterized by a drop in total energy expenditure, physical inactivity, and preference for cooler environmental temperatures, indicating a reduced body temperature set point.
-
over-expression of sEH enhances A1AR-dependent contraction and reduces KATP channel-dependent relaxation in MAs. These results suggest a possible interaction between sEH, A1AR, and KATP channels in regulating vascular tone.
-
Results indicate that the adenosine A1 receptor is an important molecular component mediating hypoxic depression in adult mice and it appears to stabilize respiration of neonatal mice
-
The findings of this study implicated a glial-neuronal circuit, mediated by Ado, neuronal AdoRA1, and glial AdK that can modulate sleep homeostasis in a manner influenced by glial metabolic state.
-
Chronic cerebral ischemia in a mouse model induced down-regulation of adenosine A1 receptors.
-
Activation of A3, A2A and A1 Adenosine Receptors in CD73-Knockout Mice Affects B16F10 Melanoma Growth, Neovascularization, Angiogenesis and Macrophage Infiltration
-
A1 receptors regulate metabolism and islet endocrine and vascular functions during ageing
-
Adenosine A1 receptor knockout mice displayed increased depressive-like behavior.
-
data support the interpretation that adenosine A receptors localized to the pontine reticular formation significantly alter nociception.
-
did not identify phenotypic modifications of A1AR-related effects on blood pressure, heart rate and plasma renin by differences in genetic background
-
Interaction between angiotensin II and adenosine in VSMC normally involves A1 receptor signalling
-
Extracellular cAMP, through its metabolite adenosine, reduced cardiomyocyte cAMP formation and hypertrophy by activating A1 adenosine receptors while delivering an antifibrotic signal to cardiac fibroblasts by A2 adenosine receptor activation.
-
NPS evokes central antinociceptive effects by activating both A1 and A2A receptors during phase 1, but only the adenosine A2A receptor during phase 2 of the formalin test
-
These findings indicate that adenosine activation of leukocyte adenosine A1 receptor plays a significant role in their recruitment to the infected lung and contributes to influenza pathogenesis.