Recombinant Human ALDH5A1
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935106861
info@markelab.com
name
Recombinant Human ALDH5A1
category
Proteins and Peptides
provider
FineTest
reference
P5328
tested applications
Western Blot,ELISA
Documents del producto
Instrucciones
Data sheet
Product specifications
| Category | Proteins and Peptides |
| Immunogen Target | 48-535 |
| Host | E.Coli |
| Origin | Human |
| Observed MW | 53.6 kDa |
| Expression | Recombinant |
| Purity | Greater than 95% by SDS-PAGE gel analyses |
| Purification | His tag |
| Size 1 | 50μg |
| Size 2 | 200μg |
| Size 3 | 1mg |
| Form | Lyophilized from a 0.2um filtered solution in PBS with 5% trehalose, pH7.4 |
| Tested Applications | Western Blot,ELISA |
| Buffer | Reconstitute with Sterile distilled water |
| Availability | 3-4 weeks |
| Storage | -20°C for 12 months as lyophilized;2-8°C for 1 month under sterile conditions after reconstitution |
| UniProt ID | P51649 |
| Alias | ALDH5A1,SSADH |
| Background | Proteins ALDH5A1 |
| Status | RUO |
| Note | This product is for research use only. |
ALDH5A1, also known as succinic semialdehyde dehydrogenase (SSADH), is a mitochondrial enzyme involved in the catabolism of gamma-aminobutyric acid (GABA), an important inhibitory neurotransmitter. ALDH5A1 catalyzes the oxidation of succinic semialdehyde (SSA) to succinate, a key intermediate in the tricarboxylic acid (TCA) cycle, linking GABA metabolism to cellular energy production. Mutations in ALDH5A1 result in succinic semialdehyde dehydrogenase deficiency, a rare autosomal recessive disorder that causes the accumulation of SSA and GABA, leading to neurological symptoms such as developmental delays, hypotonia, seizures, and ataxia. ALDH5A1 plays a crucial role in maintaining GABA homeostasis and preventing neurotoxicity. Its dysfunction highlights the importance of proper neurotransmitter balance and energy metabolism in neurological health. Therapies targeting ALDH5A1 function focus on reducing SSA accumulation and alleviating associated neurological impairments.
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