HEXA antibody

Este producto es parte de HEXA - Beta-Hexosaminidase Subunit Alpha
HEXA antibody
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Name
HEXA antibody
Category
Primary Antibodies
Provider
FineTest
Reference
FNab03843
Tested Applications
ELISA, WB

Description

Responsible for the degradation of GM2 gangliosides, and a variety of other molecules containing terminal N-acetyl hexosamines, in the brain and other tissues. The form B is active against certain oligosaccharides. The form S has no measurable activity.

Documentos del producto

Instrucciones
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Data sheet
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Especificaciones del producto

Category
Primary Antibodies
Immunogen Target
hexosaminidase A(alpha polypeptide) (HEXA)
Host
Mouse
Reactivity
Human
Recommended Dilution
WB: 1:5000 - 1:20000
Clonality
monoclonal
Conjugation
Unconjugated
Isotype
IgG2a
Clone ID
4F7
Observed MW
60 kDa
Purity
≥95% as determined by SDS-PAGE
Purification
Protein A+G purification
Size 1
100µg
Form
liquid
Tested Applications
ELISA, WB
Storage
PBS with 0.02% sodium azide and 50% glycerol pH 7.3, -20℃ for 12 months(Avoid repeated freeze / thaw cycles.)
UniProt ID
P06865
Gene ID
3073
Alias
N-acetyl-beta-glucosaminidase subunit alpha,TSD
Background
Antibody anti-HEXA
Status
RUO
Note
Mol. Weight 60 kDa

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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