Human Beta-Hexosaminidase Subunit Alpha (HEXA) Protein (Active)
1235€ (50 µg)
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name
Human Beta-Hexosaminidase Subunit Alpha (HEXA) Protein (Active)
category
Proteins and Peptides
provider
Abbexa
reference
abx691409
tested applications
SDS-PAGE
Description
Human Hexosaminidase A Protein is a recombinant protein from Human produced in Baculovirus-Insect Cells. A DNA sequence encoding the human HEXA (AAD13932.1) (Met 1-Thr 529) was fused with a polyhistidine tag at the C-terminus.
Documents del producto
Instrucciones
Data sheet
Product specifications
| Category | Proteins and Peptides |
| Immunogen Target | Hexosaminidase A |
| Host | Insect |
| Origin | Human |
| Observed MW | Molecular Weight: 59.7 kDa Sequence Fragment: Met1-Thr529 Tag: C-terminal His tag Validity: The validity for this protein is 12 months. |
| Expression | Recombinant |
| Purity | > 95% (SDS-PAGE) |
| Size 1 | 50 µg |
| Form | |
| Tested Applications | SDS-PAGE |
| Buffer | Lyophilized from sterile 20mM Tris, 500mM NaCl, pH 7.4. |
| Availability | Shipped within 5-15 working days. |
| Storage | Aliquot and store at -20°C or -80°C. Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| NCBI Accession | AAD13932.1 |
| Alias | N-acetyl-beta-glucosaminidase subunit alpha,TSD |
| Background | Protein HEXA |
| Status | RUO |
| Note | This product is for research use only. Not for human consumption, cosmetic, therapeutic or diagnostic use. |
Descripción
HEXA is the alpha subunit of the beta-hexosaminidase enzyme, a lysosomal hydrolase that catalyzes the breakdown of GM2 gangliosides into GM3 in the process of glycosphingolipid degradation The enzyme functions as a heterodimer composed of alpha and beta subunits, encoded by the HEXA and HEXB genes respectively Mutations in HEXA lead to Tay-Sachs disease, an autosomal recessive lysosomal storage disorder characterized by the accumulation of GM2 gangliosides in neuronal cells, resulting in neurodegeneration, progressive motor weakness, and developmental delay HEXA is highly active in neuronal tissues where glycosphingolipid metabolism is critical for normal brain function The absence or dysfunction of HEXA causes a loss of enzymatic activity leading to cellular toxicity and apoptosis Current therapeutic approaches include enzyme replacement therapy, substrate reduction therapy, and gene therapy to restore HEXA activity and slow disease progression
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