ALDH5A1 Antibody
Rabbit Polyclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, IHC, FC |
---|---|
Primary Accession | P51649 |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 57215 Da |
Gene ID | 7915 |
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Positive Control | Western blot: WiDr cell lysate, IHC: human brain tissue, FACS: WiDr cell lysate. |
Application & Usage | Western blot: ~1:1000, IHC: ~1:50-1:100, FACS: ~1:10-1:50. |
Other Names | ALDH5A1; SSADH; Succinate-semialdehyde dehydrogenase, mitochondrial; Aldehyde dehydrogenase family 5 members A1; NAD (+)-dependent succinic semialdehyde dehydrogenase. |
Target/Specificity | ALDH5A1 |
Antibody Form | Liquid |
Appearance | Colorless liquid |
Formulation | 100 µl of antibody in PBS with 0.09% (W/V) sodium azide |
Handling | The antibody solution should be gently mixed before use. |
Reconstitution & Storage | -20 °C |
Background Descriptions | |
Precautions | ALDH5A1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | ALDH5A1 (HGNC:408) |
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Synonyms | SSADH |
Function | Catalyzes one step in the degradation of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). |
Cellular Location | Mitochondrion. |
Tissue Location | Brain, pancreas, heart, liver, skeletal muscle and kidney. Lower in placenta |
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Provided below are standard protocols that you may find useful for product applications.
Background
Aldehyde dehydrogenases (ALDHs) mediate the NADP+-dependent oxidation of aldehydes into acids and play an important role in the detoxification of alcohol-derived acetaldehyde, as well as in lipid peroxidation and in the metabolism of corticosteroids, biogenic amines and neurotransmitters. ALDH5A1 (aldehyde dehydrogenase 5 family, member A1), also known as SSDH or SSADH, is a 535 amino acid protein that localizes to the mitochondria and belongs to the aldehyde dehydrogenase family. Expressed in a variety of tissues, including liver, heart, lung, brain, kidney and placenta, ALDH5A1 is required for gamma-aminobutyric acid (GABA) recycling from the synaptic cleft. Mutations of ALDH5A1 lead to succinate semialdehyde dehydrogenase deficiency (SSADH deficiency) that is characterized by severe ataxia and by mildly retarded psychomotor development.
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