|Datasheet||Specific References||Reviews||Related Products||Protocols|
|ORF Clone of adenosine kinase DNA.|
|Identical with the Gene Bank Ref. ID sequence.|
|Whatman FTA elute card (Cat: WB120410) contains 5-10 μg of plasmid.|
|The Whatman FTA elute card can be stored at room temperature for three months under dry condition.|
The pGEM-T is 3kb in length, and contains the amplicin resistance gene, conferring selection of the plasmid in E. coli, and the ori site which is the bacterial origin of replication. The plasmid has multiple cloning sites as shown below. The coding sequence was inserted by TA cloning. Many E. coli strains are suitable for the propagation of this vector including JM109, DH5α and TOP10.
The coding sequence can be easily obtained by digesting the vector with proper restriction enzyme(s). The coding sequence can also be amplified by PCR with M13 primers, or primer pair SP6 and T7.
|Human ADK Gene cDNA Clone (full-length ORF Clone), expression ready, FLAG-tagged||HG13149-G-F|
|Human ADK Gene cDNA Clone (full-length ORF Clone), expression ready, His-tagged||HG13149-G-H|
|Human ADK Gene cDNA Clone (full-length ORF Clone), expression ready, Myc-tagged||HG13149-G-M|
|Human ADK Gene cDNA Clone (full-length ORF Clone), expression ready, untagged||HG13149-G-N|
|Human ADK Gene cDNA Clone (full-length ORF Clone), expression ready, HA-tagged||HG13149-G-Y|
|Product name||Product name|
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.