ELISA/assay

Human NADH-ubiquinone oxidoreductase chain 6, MT-ND6 ELISA Kit

MBS936598

48-Strip-Wells

510 USD

ELISA Kit

Human NADH-ubiquinone oxidoreductase chain 6, MT-ND6 ELISA Kit

mitochondrially encoded NADH dehydrogenase 6

Human NADH-ubiquinone oxidoreductase chain 6 (MT-ND6) ELISA kit; MTND6; NADH dehydrogenase subunit 6; mitochondrially encoded NADH dehydrogenase 6

NADH dehydrogenase subunit 6 (mitochondrion); NADH-ubiquinone oxidoreductase chain 6; NADH dehydrogenase, subunit 6 (complex I); NADH dehydrogenase subunit 6; mitochondrially encoded NADH dehydrogenase 6; NADH dehydrogenase subunit 6

MT-ND6

MT-ND6; MT-ND6; MTND6; ND6; MTND6; NADH6; ND6

NU6M_HUMAN

Human

174

This assay has high sensitivity and excellent specificity for detection of human MT-ND6. No significant cross-reactivity or interference between human MT-ND6 and analogues was observed.

Unopened test kits should be stored at 2 to 8 degree C upon receipt. Please refer to pdf manual for further storage instructions.

Samples: Serum, plasma, tissue homogenates, Cell lysates. Assay Type: Sandwich. Detection Range: 23.44 pg/ml -1500 pg/ml. Sensitivity: The minimum detectable dose of human MT-ND6 is typically less than 5.86 pg/ml.The sensitivity of this assay, or Lower Limit of Detection (LLD) was defined as the lowest protein concentration that could be differentiated from zero. It was determined the mean O.D value of 20 replicates of the zero standard added by their three standard deviations.

Intra-assay Precision: Intra-assay Precision (Precision within an assay): CV%<8%. Three samples of known concentration were tested twenty times on one plate to assess. Inter-assay Precision: Inter-assay Precision (Precision between assays): CV%<10%. Three samples of known concentration were tested in twenty assays to assess.

Principle of the assay: This assay employs the quantitative sandwich enzyme immunoassay technique. Antibody specific for MT-ND6 has been pre-coated onto a microplate. Standards and samples are pipetted into the wells and any MT-ND6 present is bound by the immobilized antibody. After removing any unbound substances, a biotin-conjugated antibody specific for MT-ND6 is added to the wells. After washing, avidin conjugated Horseradish Peroxidase (HRP) is added to the wells. Following a wash to remove any unbound avidin-enzyme reagent, a substrate solution is added to the wells and color develops in proportion to the amount of MT-ND6 bound in the initial step. The color development is stopped and the intensity of the color is measured.

251831118

YP_003024037.1

NC_012920.1

P03923

18,622 Da

Electron Transport Chain Pathway (198860); Metabolism Pathway (477135); NADH:ubiquinone Oxidoreductase, Mitochondria Pathway (413406); Oxidative Phosphorylation Pathway (198870); Oxidative Phosphorylation Pathway (82942); Oxidative Phosphorylation Pathway (303); Parkinson's Disease Pathway (83098); Respiratory Electron Transport Pathway (160962); Respiratory Electron Transport, ATP Synthesis By Chemiosmotic Coupling, And Heat Production By Uncoupling Proteins. Pathway (105921); The Citric Acid (TCA) Cycle And Respiratory Electron Transport Pathway (477137)

MT-ND6: Core subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (Complex I) that is believed to belong to the minimal assembly required for catalysis. Complex I functions in the transfer of electrons from NADH to the respiratory chain. The immediate electron acceptor for the enzyme is believed to be ubiquinone. Defects in MT-ND6 are a cause of Leber hereditary optic neuropathy (LHON). LHON is a maternally inherited disease resulting in acute or subacute loss of central vision, due to optic nerve dysfunction. Cardiac conduction defects and neurological defects have also been described in some patients. LHON results from primary mitochondrial DNA mutations affecting the respiratory chain complexes. Defects in MT-ND6 are a cause of Leber hereditary optic neuropathy with dystonia (LDYT); also called familial dystonia with visual failure and striatal lucencies. LDYT is part of a spectrum of Leber hereditary optic neuropathy. It is characterized by the association of optic atrophy and central vision loss with dystonia. Defects in MT-ND6 are a cause of mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes syndrome (MELAS). MELAS is a genetically heterogenious disorder, characterized by episodic vomiting, seizures, and recurrent cerebral insults resembling strokes and causing hemiparesis, hemianopsia, or cortical blindness. Defects in MT-ND6 are a cause of mitochondrial complex I deficiency (MT-C1D). A disorder of the mitochondrial respiratory chain that causes a wide range of clinical manifestations from lethal neonatal disease to adult-onset neurodegenerative disorders. Phenotypes include macrocephaly with progressive leukodystrophy, non-specific encephalopathy, cardiomyopathy, myopathy, liver disease, Leigh syndrome, Leber hereditary optic neuropathy, and some forms of Parkinson disease. Belongs to the complex I subunit 6 family. Protein type: Membrane protein, multi-pass; EC 1.6.5.3; Oxidoreductase; Membrane protein, integral; Energy Metabolism - oxidative phosphorylation. Chromosomal Location of Human Ortholog: -. Disease: Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis, And Stroke-like Episodes; Leber Optic Atrophy

48-Strip-Wells

510 USD

96-Strip-Wells

725

5x96-Strip-Wells

2565

10x96-Strip-Wells

4800