ALDH3A2 antibody

For Research Use Only. Not for use in diagnostic procedures.

Monoclonal

IgG2b

M80549

Mouse

ALDH3A2 antibody detects endogenous levels of ALDH3A2 and does not cross-react with related proteins

Supplied in buffer containing 0.1M Tris-Glycine (pH 7.4, 150mM NaCl) with 0.2% sodium azide, 0.1% BSA and 50% glycerol

1 mg/ml (lot specific)

Store at 4 degree C for short term storage. For long term storage, store at -20 degree C.

Small volumes of anti-ALDH3A2 antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Proteases; Inhibitors; & Enzymes

Western Blot (WB)

Western blot detection of ALDH3A2 in A549,U251&HepG2 cell lysates using ALDH3A2 antibody (1:1000 diluted). Predicted band size:55KDa Observed band size:55KDa.

57,669 Da

aldehyde dehydrogenase 3 family member A2

fatty aldehyde dehydrogenase

Fatty aldehyde dehydrogenase

ALDH10; FALDH??[Similar Products]

Aldehyde dehydrogenase isozymes are thought to play a major role in the detoxification of aldehydes generated by alcohol metabolism and lipid peroxidation. This gene product catalyzes the oxidation of long-chain aliphatic aldehydes to fatty acid. Mutations in the gene cause Sjogren-Larsson syndrome. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008]

ALDH3A2: Catalyzes the oxidation of long-chain aliphatic aldehydes to fatty acids. Active on a variety of saturated and unsaturated aliphatic aldehydes between 6 and 24 carbons in length. Responsible for conversion of the sphingosine 1-phosphate (S1P) degradation product hexadecenal to hexadecenoic acid. Defects in ALDH3A2 are the cause of Sjoegren-Larsson syndrome (SLS). SLS is an autosomal recessive neurocutaneous disorder characterized by a combination of severe mental retardation, spastic di- or tetraplegia and congenital ichthyosis (increased keratinization). Ichthyosis is usually evident at birth, neurologic symptoms appear in the first or second year of life. Most patients have an IQ of less than 60. Additional clinical features include glistening white spots on the retina, seizures, short stature and speech defects. Belongs to the aldehyde dehydrogenase family. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Amino Acid Metabolism - arginine and proline; Amino Acid Metabolism - histidine; Amino Acid Metabolism - lysine degradation; Amino Acid Metabolism - tryptophan; Amino Acid Metabolism - valine, leucine and isoleucine degradation; Carbohydrate Metabolism - ascorbate and aldarate; Carbohydrate Metabolism - butanoate; Carbohydrate Metabolism - glycolysis and gluconeogenesis; Carbohydrate Metabolism - propanoate; Carbohydrate Metabolism - pyruvate; EC 1.2.1.3; Lipid Metabolism - fatty acid; Lipid Metabolism - glycerolipid; Membrane protein, integral; Mitochondrial; Other Amino Acids Metabolism - beta-alanine; Oxidoreductase; Secondary Metabolites Metabolism - limonene and pinene degradation

Chromosomal Location of Human Ortholog: 17p11.2

Cellular Component: endoplasmic reticulum membrane; intracellular membrane-bound organelle; peroxisomal membrane

Molecular Function: 3-chloroallyl aldehyde dehydrogenase activity; aldehyde dehydrogenase (NAD) activity; long-chain-alcohol oxidase activity

Biological Process: aldehyde metabolic process; central nervous system development; epidermis development; fatty acid alpha-oxidation; peripheral nervous system development; phytol metabolic process; sphingolipid biosynthetic process

Disease: Sjogren-larsson Syndrome

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