Human Beta-Hexosaminidase Subunit Alpha (HEXA) Protein
234€ (5 µg)
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Name
Human Beta-Hexosaminidase Subunit Alpha (HEXA) Protein
Category
Proteins and Peptides
Provider
Abbexa
Reference
abx073383
Tested Applications
SDS-PAGE
Description
Hexosaminidase A is a recombinant enzyme.
Documentos del producto
Instrucciones
Data sheet
Especificaciones del producto
| Category | Proteins and Peptides |
| Immunogen Target | Beta-Hexosaminidase Subunit Alpha (HEXA) |
| Host | E. coli |
| Assay Type | Activity: Not tested |
| Recommended Dilution | Optimal dilutions/concentrations should be determined by the end user. |
| Origin | Human |
| Expression | Recombinant |
| Purity | > 85% (SDS-PAGE) |
| Size 1 | 5 µg |
| Size 2 | 20 µg |
| Size 3 | 1 mg |
| Form | Liquid |
| Tested Applications | SDS-PAGE |
| Availability | Shipped within 5-10 working days. |
| Storage | Store at 4°C if the entire vial will be used within 2-4 weeks. Store at -20 °C for long term storage. For long term storage, it is recommended to add a carrier protein (0.1% HSA or BSA). Avoid repeated freeze/thaw cycles. |
| Dry Ice | No |
| UniProt ID | P06865 |
| Alias | N-acetyl-beta-glucosaminidase subunit alpha,TSD |
| Background | Protein HEXA |
| Status | RUO |
| Note | THIS PRODUCT IS FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC, THERAPEUTIC OR COSMETIC PROCEDURES. NOT FOR HUMAN OR ANIMAL CONSUMPTION. |
Background
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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