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The results of this study showed that over-expression of the major adenosine removing enzyme ADK in reactive astrocytes and subpopulation of remaining neurons in Rasmussen Encephalitis patients plays an important role in the epileptogensis of Rasmussen Encephalitis.
ADA and ADK are involved in glioma progression; increased ADA and ADK levels in peritumoral tissues may be associated with epilepsy in glioma patients.
rs11001109 rare allele homozygosity is associated with increased risk of post-traumatic epilepsy development after brain injury.
The results of this study suggest that upregulation of ADK is a common pathologic component of FCDIIB.
These results suggest that upregulation of ADK is a common pathologic hallmark of Rasmussen encephalitis and that ADK might be a target in the treatment of epilepsy associated with Rasmussen encephalitis.
Data show that we a significantly higher expression of ADK in the peritumoral infiltrated tissue of patients with epilepsy than in patients without epilepsy.
The results of this study suggested that dysregulation of ADK in astrocytes is a common pathologic hallmark of temporal lobe epilepsy.
The cytoplasmic isoform of adenosine kinase is sufficient to alter sleep physiology. ADK might orchestrate neurotransmitter pathways involved in the generation of electroencephlogram oscillations and regulation of sleep.
The catalytic properties, gene expression and protein levels of certain proteins involved in mitochondrial ATP synthesis, such as F1F0-ATPase, ANT and AK, in human skin fibroblasts with trisomic karyotype, compared them with euploid fibroblasts.
Equilibrative nucleoside transporters (hENT1, hENT2) together with adenosine kinase and 5'-nucleotidase play a crucial role in the regulation of CFTR through an adenosine-dependent pathway in human airway epithelia.
role for HIF-1alpha in transcriptional repression of AK in hypoxia
adenosine kinase gene expression was significantly higher in cancer than in normal-appearing tissue, in line with our previous measurements of adenosine kinase enzyme activities in colorectal tumor samples
both deoxycytidine kinase and adenosine kinase are involved in this model of ADA deficiency
This study reports for the first time subcellular localization of the enzyme AdK in mammalian cells.
Adenosine kinase contributes to cytokinin homeostasis
Increased cytokinin-responsive promoter activity in Arabidopsis plant tissue may therefore be a consequence of an ADK/AL2/C2 interaction.
Metabolic and growth alterations of A. thaliana with a knockout mutation of this site.
Augmentation of intracellular adenosine levels through ADK knockout in myeloid cells protects ApoE(-/-) mice against atherosclerosis by reducing foam cell formation via the epigenetic regulation of cholesterol trafficking.
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.
These results suggest that mice with ADK deficiency have reduced bone formation due to increased osteoclastogenesis and bone resorption.
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.
ADK expression negatively regulates the adaptive beta-cell response to high-fat diet challenge.
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.
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.
We conclude that ADK provides important upstream regulation of adenosine-based homeostatic function of the brain
Adenosine kinase inhibition selectively promotes rodent and porcine islet beta-cell replication
Knockdown of Adk can protect the brain from the effects of a stroke.
a complete absence of ADK led to abnormalities in hepatic adenosine metabolism and to the development of acute, severe neonatal hepatic steatosis.
adenosine kinase inhibition promotes survival of fetal adenosine deaminase-deficient thymocytes by blocking dATP accumulation
Overexpression of adenosine kinase in discrete parts of the epileptic hippocampus may contribute to the development and progression of seizure activity.
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.
transient downregulation of hippocampal ADK after stroke might be a protective mechanism during maturation hippocampal cell loss.
The results of this study confirmed that ADK overexpression could lead to functional concomitant alterations in dopaminergic and glutamatergic functions.
These findings suggest that astrocyte-based ADK provides a critical link between astrogliosis and neuronal dysfunction in epilepsy.
This gene an enzyme which catalyzes the transfer of the gamma-phosphate from ATP to adenosine, thereby serving as a regulator of concentrations of both extracellular adenosine and intracellular adenine nucleotides. Adenosine has widespread effects on the cardiovascular, nervous, respiratory, and immune systems and inhibitors of the enzyme could play an important pharmacological role in increasing intravascular adenosine concentrations and acting as anti-inflammatory agents. Multiple transcript variants encoding different isoforms have been found for this gene.
, adenosine kinase (short isoform)-like protein
, adenosine kinase
, Adenosine kinase
, adenosine kinase-like
, Adenosine 5'-phosphotransferase
, adenosine kinase S homeolog