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

Polyclonal

Rabbit

Affinity purified

Liquid

100ug/100ul (lot specific)

This product is stable for several weeks at 4 degree C as an undiluted liquid. Dilute only prior to immediate use. For extended storage, aliquot contents and freeze at -20 degree C or below. Avoid cycles of freezing and thawing. Expiration date is one (1) year from date of receipt.

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.

Rabbit polyclonal ALDH3A2(

Western Blot (WB), Immunohistochemistry (IHC)

ELISA titer: 1:20,000-1:80,000
Western blot analysis: 1:1,000-1:2,000
Immunohistochemistry: 1:100-1:500
Optimal dilutions/concentrations should be determined by the end user.

57,669 Da

aldehyde dehydrogenase 3 family, member A2

fatty aldehyde dehydrogenase; aldehyde dehydrogenase 10; aldehyde dehydrogenase family 3 member A2; microsomal aldehyde dehydrogenase

Fatty aldehyde dehydrogenase

AL3A2_HUMAN

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

Chromosomal Location of Human Ortholog: 17p11.2

Cellular Component: endoplasmic reticulum membrane; intracellular membrane-bound organelle; mitochondrial inner membrane; integral to membrane; peroxisome

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

Biological Process: phytol metabolic process; epidermis development; central nervous system development; aldehyde metabolic process; sesquiterpenoid metabolic process; peripheral nervous system development

Disease: Sjogren-larsson Syndrome

(1) Shimada,M., Miyagawa,T., Kawashima,M., et al. An approach based on a genome-wide association study reveals candidate loci for narcolepsy. Hum. Genet. 128 (4), 433-441 (2010).

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