GALE Mouse Monoclonal Antibody [Clone ID: OTI1C4]
CAT#: TA502146
GALE mouse monoclonal antibody, clone OTI1C4 (formerly 1C4)
Size: 30 ul
Formulation: Carrier Free
Specifications
Product Data | |
Clone Name | OTI1C4 |
Applications | IHC, WB |
Recommended Dilution | WB 1:500~2000, IHC 1:150 |
Reactivities | Human, Monkey, Mouse, Rat, Dog |
Host | Mouse |
Isotype | IgG1 |
Clonality | Monoclonal |
Immunogen | Full length human recombinant protein of human GALE (NP_000394) produced in HEK293T cell. |
Formulation | PBS (PH 7.3) containing 1% BSA, 50% glycerol and 0.02% sodium azide. |
Concentration | 1 mg/ml |
Purification | Purified from mouse ascites fluids or tissue culture supernatant by affinity chromatography (protein A/G) |
Conjugation | Unconjugated |
Storage | Store at -20°C as received. |
Stability | Stable for 12 months from date of receipt. |
Predicted Protein Size | 38.1 kDa |
Gene Name | UDP-galactose-4-epimerase |
Database Link | |
Background | This gene encodes UDP-galactose-4-epimerase which catalyzes two distinct but analogous reactions: the epimerization of UDP-glucose to UDP-galactose, and the epimerization of UDP-N-acetylglucosamine to UDP-N-acetylgalactosamine. The bifunctional nature of the enzyme has the important metabolic consequence that mutant cells (or individuals) are dependent not only on exogenous galactose, but also on exogenous N-acetylgalactosamine as a necessary precursor for the synthesis of glycoproteins and glycolipids. Mutations in this gene result in epimerase-deficiency galactosemia, also referred to as galactosemia type 3, a disease characterized by liver damage, early-onset cataracts, deafness and mental retardation, with symptoms ranging from mild ('peripheral' form) to severe ('generalized' form). Multiple alternatively spliced transcripts encoding the same protein have been identified. [provided by RefSeq, Jul 2008] |
Synonyms | SDR1E1 |
Reference Data | |
Protein Families | Druggable Genome |
Protein Pathways | Amino sugar and nucleotide sugar metabolism, Galactose metabolism, Metabolic pathways |
Documents
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Resources
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