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ADK  Protein

All ADK Reagents

Expression host: Baculovirus-Insect Cells  
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13149-H20B-50
50 µg 
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ADK Related Pathways

ADK Summary & Protein Information

ADK Background

Gene Summary: This ADK 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. [provided by RefSeq, Jan 2011]
General information above from NCBI
Catalytic activity: ATP + adenosine = ADP + AMP.
Cofactor: Binds 3 magnesium ions per subunit.
Subunit structure: Monomer.
Tissue specificity: Widely expressed. Highest level in placenta, liver, muscle and kidney.
Involvement in disease: Hypermethioninemia due to adenosine kinase deficiency (HMAKD) [MIM:614300]: A metabolic disorder characterized by global developmental delay, early-onset seizures, mild dysmorphic features, and characteristic biochemical anomalies, including persistent hypermethioninemia with increased levels of S- adenosylmethionine and S-adenosylhomocysteine. Homocysteine levels are typically normal. Note=The disease is caused by mutations affecting the gene represented in this entry.
Sequence similarity: Belongs to the carbohydrate kinase PfkB family.
General information above from UniProt

Adenosine kinase(ADK) belongs to the family of transferases. Adenosine kinase (ADK) is the key enzyme in adenosine metabolism and catalyzes ATP and adenosine into two products: ADP and AMP. Two isoforms of the enzyme adenosine kinase (ADK), which differ at their N-terminal ends, are found in mammalian cells. It has been shown that the two ADK isoforms differ only in their first exons and the promoter regions; hence they arise via differential splicing of their first exons with the other exons common to both isoforms. In adult brain, ADK is primarily present in astrocytes. Several lines of experimental evidence support a critical role of ADK in different types of brain injury associated with astrogliosis, which is also a prominent morphologic feature of temporal lobe epilepsy (TLE). It has been suggested that dysregulation of ADK in astrocytes is a common pathologic hallmark of TLE. Moreover, in vitro data suggest the existence of an additional layer of modulatory crosstalk between the astrocyte-based adenosine cycle and inflammation. ADK also contributes to CK homeostasis in vivo. 

ADK Alternative Name

AK, [homo-sapiens]
AK, [human]
2310026J05Rik,5033405D03Rik,AI255373,AI987814,Ak,MGC6593, [mouse]
Ak,AI255373,AI987814,2310026J05Rik,5033405D03Rik, [mus-musculus]

ADK Related Studies

  • Aronica E, et al. (2011) Upregulation of adenosine kinase in astrocytes in experimental and human temporal lobe epilepsy. Epilepsia.52 (9): 1645-55.
  • Kuettel S, et al. (2011) Crystal structures of T. b. rhodesiense adenosine kinase complexed with inhibitor and activator: implications for catalysis and hyperactivation. PLoS Negl Trop Dis. 5 (5): e1164.
  • Cui XA, et al. (2011) Molecular characterization of Chinese hamster cells mutants affected in adenosine kinase and showing novel genetic and biochemical characteristics. BMC Biochem. 12 (1): 22.
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