Product nameAnti-NADH dehydrogenase subunit 4 antibody [9E4-2D8] - N-terminal
DescriptionMouse monoclonal [9E4-2D8] to NADH dehydrogenase subunit 4 - N-terminal
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Human
Synthetic peptide corresponding to Human NADH dehydrogenase subunit 4 (N terminal).
Database link: P03905
- WB: Mitochondria from cultured normal control human dermal fibroblasts neonatal (HDFn).
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.20
Preservative: 0.02% Sodium azide
Constituents: 0.36% HEPES, 0.87% Sodium chloride
Concentration information loading...
PurityProtein L purified
Purification notesPurified from hybridoma cell culture supernatant by Protein L affinity chromatography from fetal bovine serum containing medium (Protein L does not bind bovine IgG).
Light chain typekappa
- Pathways and Processes
- Metabolic signaling pathways
- Energy transfer pathways
- Integration of energy
Our Abpromise guarantee covers the use of ab219822 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use a concentration of 4 µg/ml. Detects a band of approximately 37 kDa (predicted molecular weight: 52 kDa).
Western blot using whole cell extracts is not recommended.
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-ND4 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-ND4 are a cause of Leber hereditary optic neuropathy with dystonia (LDYT) [MIM:500001]; 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-ND4 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 4 family.
Cellular localizationMitochondrion membrane.
- Information by UniProt
- MT-ND4 antibody
- MTND4 antibody
- NADH dehydrogenase subunit 4 antibody
All lanes : Anti-NADH dehydrogenase subunit 4 antibody [9E4-2D8] - N-terminal (ab219822) at 4 µg/ml
Lane 1 : Mitochondria from cultured normal control human dermal fibroblasts neonatal (HDFn)
Lane 2 : Mitochondria from HDFn cells depleted of mtDNA by long-term proliferation in the presence of ethidium bromide
Lysates/proteins at 10 µg per lane.
All lanes : HRP-labeled Goat-anti-mouse IgG
Developed using the ECL technique.
Predicted band size: 52 kDa
Observed band size: 37 kDa why is the actual band size different from the predicted?
Mitochondrial proteins solubilized in 2% SDS were separated by SDS-PAGE and then transferred to PVDF membranes in CAPS buffer.
ab219822 has not yet been referenced specifically in any publications.