2.7.1.20: adenosine kinase
This is an abbreviated version!
For detailed information about adenosine kinase, go to the full flat file.
Word Map on EC 2.7.1.20
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2.7.1.20
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nucleoside
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deaminase
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purine
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amp
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adenylate
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inosine
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salvage
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hypoxanthine
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epilepsy
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phosphoribosyltransferase
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5'-nucleotidase
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5-iodotubercidin
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riboside
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deoxyadenosine
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s-adenosylhomocysteine
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deoxycytidine
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aicar
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anticonvulsant
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tubercidin
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dipyridamole
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neuromodulator
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ehna
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2\'-deoxycoformycin
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ecto-5\'-nucleotidase
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ribokinase
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erythro-9-2-hydroxy-3-nonyl
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adenosinergic
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6-methylmercaptopurine
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3hadenosine
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2-chloroadenosine
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coformycin
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nitrobenzylthioinosine
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epileptogenesis
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hypoxanthine-guanine
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transmethylation
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adenosine-induced
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hgprt
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kinase-deficient
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2'-deoxyadenosine
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adenosine-mediated
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3.5.4.4
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deoxycoformycin
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non-nucleoside
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analysis
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2.4.2.8
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9-beta-d-arabinofuranosyladenine
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n6-cyclopentyladenosine
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erythro-9-2-hydroxy-3-nonyladenine
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dado
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ara-a
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medicine
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diagnostics
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rephosphorylation
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pharmacology
- 2.7.1.20
- nucleoside
- deaminase
- purine
- amp
- adenylate
- inosine
-
salvage
- hypoxanthine
- epilepsy
-
phosphoribosyltransferase
- 5'-nucleotidase
- 5-iodotubercidin
- riboside
- deoxyadenosine
- s-adenosylhomocysteine
- deoxycytidine
- aicar
-
anticonvulsant
- tubercidin
- dipyridamole
-
neuromodulator
- ehna
-
2\'-deoxycoformycin
-
ecto-5\'-nucleotidase
- ribokinase
-
erythro-9-2-hydroxy-3-nonyl
-
adenosinergic
- 6-methylmercaptopurine
-
3hadenosine
- 2-chloroadenosine
- coformycin
-
nitrobenzylthioinosine
-
epileptogenesis
-
hypoxanthine-guanine
-
transmethylation
-
adenosine-induced
- hgprt
-
kinase-deficient
- 2'-deoxyadenosine
-
adenosine-mediated
-
3.5.4.4
- deoxycoformycin
-
non-nucleoside
- analysis
-
2.4.2.8
- 9-beta-d-arabinofuranosyladenine
-
n6-cyclopentyladenosine
-
erythro-9-2-hydroxy-3-nonyladenine
-
dado
- ara-a
- medicine
- diagnostics
-
rephosphorylation
- pharmacology
Reaction
Synonyms
adenosine kinase (phosphorylating), ADK, AdK-L, AdK-S, Ado kinase, AdoK, AK, ATP:adenosine 5'-phosphotransferase, CpAK, hADK, kinase, adenosine (phosphorylating), LdAdK, MGG_06270, Rv2202c, Tb927.6.2360, TbAK
ECTree
2.7.1.20 adenosine kinaseAdvanced search results
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results (Source Tissue
Source Tissue on EC 2.7.1.20 - adenosine kinase
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SOURCE TISSUE 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
SOURCE
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adenosine kinase gene expression is significantly higher in cancer than in normal-appearing tissue
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T-lymphoblast cell lines MILT 4F, CCRF CEM and RPMI 8402, B-lymphoblast cell lines BALL 1 and EBV (Epstein-Barr-virus)-transformed B-lymphoblast
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ADK expression in young neurons may provide a salvage pathway to utilize adenosine in nucleic acid synthesis
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expanding green siliques contain a 4fold higher expression of isozyme ADK1 compared to isozyme ADK2
additional information
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astrocyte-based ADK provides a critical link between astrogliosis and neuronal dysfunction in epilepsy
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surgically resected human epileptic cortical specimens from Rasmussen encephalitis patients
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at early postnatal stages ADK immunoreactivity is prominent in neurons, notably in cerebral cortex and hippocampus. Thereafter, adenosine kinase gradually disappears from neurons and appears in newly developed nestin- and glial fibrillary acidic protein-positive astrocytes. The region-specific downregulation of neuronal adenosine kinase coincides with the onset of myelination. After postnatal day 14, the transition from neuronal to astrocytic ADK expression is complete, except in a subset of neurons that retain ADK until adulthood in specific regions, such as the striatum
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low levels of adenosine kinase are essential to maintain adenosine-mediated endogenous neuroprotection and pathologic increases in ADK may render the brain more susceptible to injury
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transgenic overexpression of adenosine kinase in brain leads to multiple learning impairments and altered sensitivity to psychomimetic drugs
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transgenic overexpression of ADK, which reduces adenosine in mouse brain, results in increased levels of myelin proteolipid protein
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enzyme activity decreases by 5.5fold in senescent cell cultures, 1.5-3.5fold increased activity of both isozymes during cell wall synthesis
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transient downregulation of hippocampal ADK after stroke might be a protective mechanism during maturation hippocampal cell loss
additional information
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tissue expression level analysis, the isozymes have similar expression patterns, except in case of microgametogenesis, where isozyme ADK1 is upregulated while isozyme ADK2 is not, ADK1 is the major isozyme
additional information
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transcript profiling, during desiccation the enzyme expression level remains constant up to 18-20 days after pollination, then decreases, overview
additional information
analysis of modulation of the expression patterns of isozymes ADK1S, ADK1T, ADK2S, and ADK2T during the cell cycle, overview
additional information
analysis of modulation of the expression patterns of isozymes ADK1S, ADK1T, ADK2S, and ADK2T during the cell cycle, overview
additional information
analysis of modulation of the expression patterns of isozymes ADK1S, ADK1T, ADK2S, and ADK2T during the cell cycle, overview
additional information
analysis of modulation of the expression patterns of isozymes ADK1S, ADK1T, ADK2S, and ADK2T during the cell cycle, overview
additional information
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analysis of modulation of the expression patterns of isozymes ADK1S, ADK1T, ADK2S, and ADK2T during the cell cycle, overview
additional information
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transcript profiling of isozymes ADK1 and ADK2, during desiccation the enzyme expression level remains constant up to 27 days after pollination, then decreases, and peaking again at day 43, then decreases again, overview
