Product nameMT-ND1 peptide
See all MT-ND1 proteins and peptides
Our Abpromise guarantee covers the use of ab195040 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Blocking - Blocking peptide for Anti-MT-ND1 antibody [EPR13466(2)] (ab181848)
This is the blocking peptide for ab181848
- First try to dissolve a small amount of peptide in either water or buffer. The more charged residues on a peptide, the more soluble it is in aqueous solutions.
- If the peptide doesn’t dissolve try an organic solvent e.g. DMSO, then dilute using water or buffer.
- Consider that any solvent used must be compatible with your assay. If a peptide does not dissolve and you need to recover it, lyophilise to remove the solvent.
- Gentle warming and sonication can effectively aid peptide solubilisation. If the solution is cloudy or has gelled the peptide may be in suspension rather than solubilised.
- Peptides containing cysteine are easily oxidised, so should be prepared in solution just prior to use.
Concentration information loading...
Preparation and Storage
Stability and Storage
Shipped at 4°C. Store at -20°C.
- Complex I, subunit ND1
- Mitochondrially encoded NADH dehydrogenase 1
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-ND1 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-ND1 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.
Defects in MT-ND1 may be associated with susceptibility to Alzheimer disease mitochondrial (AD-MT) [MIM:502500]. Alzheimer disease is a neurodegenerative disorder characterized by progressive dementia, loss of cognitive abilities, and deposition of fibrillar amyloid proteins as intraneuronal neurofibrillary tangles, extracellular amyloid plaques and vascular amyloid deposits. The major constituent of these plaques is the neurotoxic amyloid-beta-APP 40-42 peptide (s), derived proteolytically from the transmembrane precursor protein APP by sequential secretase processing. The cytotoxic C-terminal fragments (CTFs) and the caspase-cleaved products such as C31 derived from APP, are also implicated in neuronal death.
Defects in MT-ND1 may be associated with non-insulin-dependent diabetes mellitus (NIDDM).
Sequence similaritiesBelongs to the complex I subunit 1 family.
Cellular localizationMitochondrion inner membrane.
- Information by UniProt
ab195040 has not yet been referenced specifically in any publications.