|Datasheet||Specific References||Reviews||Related Products||Protocols|
|ORF Clone of Homo sapiens aldehyde dehydrogenase 7 family, member A1 DNA.|
|EPD, PDE, ATQ1, FLJ11738, FLJ92814, ALDH7A1|
|pMD18-T Simple Vector|
|Identical with the Gene Bank Ref. ID sequence except for the point mutation 1231 A/C resulting in the amino acid Lys substitution by Gln.|
|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.|
pMD18-T Simple Vector is a high-efficiency TA cloning vector constructed from pUC18, of which the initial multiple cloning sites (MCS) were destroyed. Thus the cDNA should be amplified by PCR with primers containing a restriction site for subclone. Competent cells appropriate for pUC18 are also appropriated for the Vector, e.g. JM109, DH5α, TOP10. The pMD18-T Simple Vector is 2.6kb in size. Selection of the plasmid in E. coli is conferred by the ampicillin resistance gene. The coding sequence was inserted by TA cloning at site 425.
The coding sequence can be amplified by PCR with M13-47 and RV-M primers.
|Human ALDH7A1 Gene cDNA Clone (full-length ORF Clone), expression ready, FLAG-tagged||HG11614-M-F|
|Human ALDH7A1 Gene cDNA Clone (full-length ORF Clone), expression ready, His-tagged||HG11614-M-H|
|Human ALDH7A1 Gene cDNA Clone (full-length ORF Clone), expression ready, Myc-tagged||HG11614-M-M|
|Human ALDH7A1 Gene cDNA Clone (full-length ORF Clone), expression ready, untagged||HG11614-M-N|
|Human ALDH7A1 Gene cDNA Clone (full-length ORF Clone), expression ready, HA-tagged||HG11614-M-Y|
|Product name||Product name|
ALDH7A1 (Aldehyde dehydrogenase 7 family, member A1) is a member of subfamily 7 in the aldehyde dehydrogenase family. These enzymes are thought to play a major role in the detoxification of aldehydes generated by alcohol metabolism and lipid peroxidation. Mammalian ALDH7A1 is homologous to plant ALDH7B1 which protects against various forms of stress such as increased salinity, dehydration and treatment with oxidants or pesticides. In mammals, ALDH7A1 is known to play a primary role during lysine catabolism through the NAD+-dependent oxidative conversion of aminoadipate semialdehyde (AASA) to its corresponding carboxylic acid, α-aminoadipic acid. Deleterious mutations in human ALDH7A1 are responsible for pyridoxine-dependent and folinic acid-responsive seizures. ALDH7A1 is a novel aldehyde dehydrogenase expressed in multiple subcellular compartments that protects against hyperosmotic stress by generating osmolytes and metabolizing toxic aldehydes.