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results demonstrate a key developmental role of ADK in mediating behaviors in adulthood related to neuropsychiatric disease and support the greater prevalence of these disorders among males.
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These results suggest that mice with ADK deficiency have reduced bone formation due to increased osteoclastogenesis and bone resorption.
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Here the authors show that pro-inflammatory stimuli lead to endothelial inflammation by increasing adenosine kinase expression, and that its knockdown in endothelial cells inhibits atherosclerosis and cerebral ischemic injury in mice.
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ADK expression negatively regulates the adaptive beta-cell response to high-fat diet challenge.
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Our data show that neurological phenotypes in ADK-deficient patients are intrinsic to ADK deficiency in the brain and that blocking A2AR activity therapeutically can attenuate neurological symptoms in ADK deficiency.
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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.
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We conclude that ADK provides important upstream regulation of adenosine-based homeostatic function of the brain
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Adenosine kinase inhibition selectively promotes rodent and porcine islet beta-cell replication
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Knockdown of Adk can protect the brain from the effects of a stroke.
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a complete absence of ADK led to abnormalities in hepatic adenosine metabolism and to the development of acute, severe neonatal hepatic steatosis.
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adenosine kinase inhibition promotes survival of fetal adenosine deaminase-deficient thymocytes by blocking dATP accumulation
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Overexpression of adenosine kinase in discrete parts of the epileptic hippocampus may contribute to the development and progression of seizure activity.
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Data report the cloning of two isoforms of adenosine kinase from a mouse brain cDNA library, and the role of these isoenzymes as sustrates for phosphorylation were examined.
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transient downregulation of hippocampal ADK after stroke might be a protective mechanism during maturation hippocampal cell loss.
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The results of this study confirmed that ADK overexpression could lead to functional concomitant alterations in dopaminergic and glutamatergic functions.
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These findings suggest that astrocyte-based ADK provides a critical link between astrogliosis and neuronal dysfunction in epilepsy.
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role for HIF-1alpha in transcriptional repression of AK in hypoxia
