Cat#:PA-3200F;Product Name:Rabbit Anti-Lipoamide Dehydrogenase Antibody;Synonym:Lipoamide Dehydrogenase; Diaphorase; Dihydrolipoamide dehydrogenase; Dihydrolipoyl dehydrogenase; DLD; Dihydrolipoyl dehydrogenase mitochondrial; DLDH; E3; E3 component of pyruvate dehydrogenase; E3 component of pyruvate dehydrogenase complex 2 oxo glutarate complex branched chain keto acid dehydrogenase complex; GCSL; Glycine cleavage system L protein; Glycine cleavage system protein L; LAD; Lipoamide reductase; Lipoyl dehydrogenase; PHE 3; PHE3; EC=1.8.1.4; Lipoamide Dehydrogenase; DTD; DTD HUMAN; DT DIAPHORASE; DT DIAPHORASE HUMAN; DIAPHORASE; EC 1.8.1.4 TYPE III; EC 1.8.1.4; EC 1.6.99; EC: 1.6.99; EC 1.6.99.2; IUB: 1.6.99.1; QUINONE REDUCTASE; QUINONE REDUCTASE HUMAN; Diaphorase Clostridium kluyveri; DT Diaphorase from rat; DTD, NQO1, Quinone reductase;Background:Lipoamide dehydrogenase or dihydrolipoamide dehydrogenase (DLD) is a component of the glycine cleavage system as well as of the alpha ketoacid dehydrogenase complexes. It is a homodimer. It belongs to the class I pyridine nucleotide disulfide oxidoreductase family. Defects in DLD are a cause of congenital infantile lactic acidosis. Moreover, defects in DLD are the cause of DLD deficiency; which results in extensive metabolic disturbances, including lactic acidemia, Krebs cycle dysfunction, and impaired branched amino acid degradation. DLD deficiency also causes neurological degeneration due to the sensitivity of the central nervous system to defects in oxidative metabolism.;Description:Rabbit Anti-Lipoamide Dehydrogenase Polyclonal Antibody;Host Species:Rabbit;Species Reactivity:Parasite;Isotype:IgG1;Application:ELISA, IEP;Storage:Store antibody products at 2-8°C. For long term storage, aliquot and freeze at -20°C. Avoid repeated freeze/thaw cycles;Usage:For Lab Research Use Only;
Lipoamide dehydrogenase or dihydrolipoamide dehydrogenase (DLD) is a component of the glycine cleavage system as well as of the alpha ketoacid dehydrogenase complexes. It is a homodimer. It belongs to the class I pyridine nucleotide disulfide oxidoreductase family. Defects in DLD are a cause of congenital infantile lactic acidosis. Moreover, defects in DLD are the cause of DLD deficiency; which results in extensive metabolic disturbances, including lactic acidemia, Krebs cycle dysfunction, and impaired branched amino acid degradation. DLD deficiency also causes neurological degeneration due to the sensitivity of the central nervous system to defects in oxidative metabolism.