Anti-Hydroxysteroid (17-beta) Dehydrogenase 4/HSD17B4 Antibody Picoband® Fluoro647 Conjugated

Peroxisomal multifunctional enzyme type 2 is a protein that in humans is encoded by the HSD17B4 gene. The protein encoded by this gene is a bifunctional enzyme that is involved in the peroxisomal beta-oxidation pathway for fatty acids. It also acts as a catalyst for the formation of 3-ketoacyl-CoA intermediates from both straight-chain and 2-methyl-branched-chain fatty acids. Defects in this gene that affect the peroxisomal fatty acid beta-oxidation activity are a cause of D-bifunctional protein deficiency (DBPD) . An apparent pseudogene of this gene is present on chromosome 8. Multiple alternatively spliced transcript variants encoding distinct isoforms have been found for this gene.

Peroxisomal multifunctional enzyme type 2; MFE-2;17-beta-hydroxysteroid dehydrogenase 4;17-beta-HSD 4; D-bifunctional protein; DBP; Multifunctional protein 2; MPF-2; Short chain dehydrogenase/reductase family 8C member 1; (3R) -hydroxyacyl-CoA dehydrogenase;1.1.1.n12; Enoyl-CoA hydratase 2;4.2.1.107;4.2.1.119;3-alpha,7-alpha,12-alpha-trihydroxy-5-beta-cholest-24-enoyl-CoA hydratase; HSD17B4; EDH17B4, SDR8C1

E.coli-derived human HSD17B4 recombinant protein (Position: D510-L736) . Human HSD17B4 shares 87.7% and 89% amino acid (aa) sequence identity with mouse and rat HSD17B4, respectively.

Cancer, Cardiovascular, Fatty Acid Oxidation, Fatty Acids, Lipid and Lipoprotein Metabolism, Lipid Metabolism, Lipids/Lipoproteins, Metabolic Signaling Pathways, Metabolism, Pathways and Processes, Redox Metabolism, Signal Transduction, Tumor Biomarkers

Bifunctional enzyme acting on the peroxisomal beta- oxidation pathway for fatty acids. Catalyzes the formation of 3- ketoacyl-CoA intermediates from both straight-chain and 2-methyl- branched-chain fatty acids. .

1. Entrez Gene: HSD17B4 Hydroxysteroid (17-beta) dehydrogenase 1. 2. Aka JA, Mazumdar M, Chen CQ, Poirier D, Lin SX (Apr 2010) . 17beta-hydroxysteroid dehydrogenase type 1 stimulates breast cancer by dihydrotestosterone inactivation in addition to estradiol production.Molecular Endocrinology. 24 (4) : 832–45.