AGA / ASRG / Aspartylglucosaminidase Protein Product Information

Synonym : AGA
Protein Construction: A DNA sequence encoding the human AGA (CAA39029.1) (Met1-Ile346) was expressed with a C-terminal polyhistidine tag.
Source: Human
Expression Host: Human Cell

AGA / ASRG / Aspartylglucosaminidase Protein QC Testing

Purity: (5.2+44.1+46.8+3.4) % as determined by SDS-PAGE SDS-PAGE
Endotoxin: < 1.0 EU per μg of the protein as determined by the LAL method
Stability: Samples are stable for up to twelve months from date of receipt at -70℃
Predicted N terminal: Ser 24
Molecular Mass: The recombinant human AGA comprises 334 amino acids and has a predicted molecular mass of 36.1 kDa. The apparent molecular mass of the protein is approximately 47, 29, 23 and 20 kDa in SDS-PAGE under reducing conditions due to glycosylation.
Formulation: Lyophilized from sterile PBS, pH 7.4.
                 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.

AGA / ASRG / Aspartylglucosaminidase Protein Usage Guide

Storage:  Store it under sterile conditions at -70℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
Reconstitution:  A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.

AGA / ASRG / Aspartylglucosaminidase Protein Description

ASRG, also known as aspartylglucosaminidase, is a lysosomal amidase that hydrolyzes the N- acetylglucosamine -asparagine linkage as one of the final steps in the breakdown of glycoproteins. ASRG cleaves asparagine from N-acetylglucosamines as one of the final steps in the lysosomal breakdown of glycoproteins. The lysosomal storage disease aspartylglycosaminuria is caused by a deficiency in ASRG. Aspartylglycosaminuria is an inborn lysosomal storage disease. Clinical features of aspartylglycosaminuria include mild to severe mental retardation manifesting from the age of 2, coarse facial features and mild connective tissue abnormalities.

References

Ikonen E. et al., 1991, EMBO J. 10 (1): 51-8.
Enomaa N. et al., 1992, Biochem J. 286 (2): 613-8.
Mononen I. et al., 1993, FASEB J. 7 (13): 1247-56.
Enomaa NE. et al., 1993, J Histochem Cytochem. 41 (7): 981-9.

規(guī)格:20ug

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