Key features and details
- Rabbit polyclonal to MT-ND5
- Suitable for: WB
- Reacts with: Human
- Isotype: IgG
Product nameAnti-MT-ND5 antibody
See all MT-ND5 primary antibodies
DescriptionRabbit polyclonal to MT-ND5
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Human
Synthetic peptide derived from an internal region of Human MT-ND5
- Jurkat cell lysate
Storage instructionsShipped at 4°C. Store at -20ºC.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Constituents: 49% PBS, 0.88% Sodium chloride, 50% Glycerol
PBS is without Mg2+ and Ca2+
Concentration information loading...
PurityImmunogen affinity purified
Purification notesab138136 was affinity purified from rabbit antiserum by immunogenic peptide affinity chromatography.
Our Abpromise guarantee covers the use of ab138136 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/500 - 1/1000. Predicted molecular weight: 67 kDa.|
FunctionCore 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.
Involvement in diseaseDefects in MT-ND5 are a cause of Leber hereditary optic neuropathy (LHON) [MIM:535000]. 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) [MIM:256000]. 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) [MIM:252010]. 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) [MIM:540000]. MELAS is a genetically heterogenious disorder, characterized by episodic vomiting, seizures, and recurrent cerebral insults resembling strokes and causing hemiparesis, hemianopsia, or cortical blindness.
Sequence similaritiesBelongs to the complex I subunit 5 family.
Cellular localizationMitochondrion inner membrane.
- Information by UniProt
- Complex I, subunit ND5 antibody
- EC 126.96.36.199 antibody
- Mitochondrially encoded NADH dehydrogenase 5 antibody
ab138136 has not yet been referenced specifically in any publications.