|Datasheet||Specific References||Reviews||Related Products||Protocols|
|ATQ1, EPD, FLJ11738, FLJ92814, PDE, ALDH7A1|
|A DNA sequence encoding the human ALDH7A1 isoform 2 (P49419-2) (Ser 2-Gln 511) was expressed, with a polyhistide tag at the N-terminus.|
|In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature.|
Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise.
|> 93 % as determined by SDS-PAGE|
|Please contact us for more information.|
|Samples are stable for up to twelve months from date of receipt at -70℃|
|The recombinant human ALDH7A1 consisting of 517 amino acids and migrates as an approximately 56 kDa band in SDS-PAGE under reducing conditions as predicted.|
|Lyophilized from sterile 50mM Tris, 500mM NaCl, 20% glycerol, pH 8.0|
1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
2. Please contact us for any concerns or special requirements.
|Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.|
|A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.|
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.