Rabbit anti-Human NADH Dehydrogenase 5 (ND5) Polyclonal Antibody | anti-ND5 antibody
PE-Linked Polyclonal Antibody to NADH Dehydrogenase 5 (ND5)
Avoid repeated freeze/thaw cycles.
The thermal stability is described by the loss rate. The loss rate was determined by accelerated thermal degradation test, that is, incubate the protein at 37 degree C for 48h, and no obvious degradation and precipitation were observed. The loss rate is less than 5% within the expiration date under appropriate storage condition.
NCBI and Uniprot Product Information
Uniprot Description
MT-ND5: 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-ND5 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-ND5 are a cause of Leigh syndrome (LS). LS is a severe neurological disorder characterized by bilaterally symmetrical necrotic lesions in subcortical brain regions. Defects in MT-ND5 are a cause of mitochondrial complex I deficiency (MT-C1D). A disorder of the mitochondrial respiratory chain that causes a wide range of clinical disorders, 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. Defects in MT-ND5 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. Belongs to the complex I subunit 5 family.
Protein type: Membrane protein, integral; EC 1.6.5.3; Oxidoreductase; Mitochondrial; Membrane protein, multi-pass
Chromosomal Location of Human Ortholog: -
Disease: Mitochondrial Myopathy, Encephalopathy, Lactic Acidosis, And Stroke-like Episodes; Leber Optic Atrophy
