Anti-MT-ND5 antibody (ab138136)
Key features and details
- Rabbit polyclonal to MT-ND5
- Suitable for: WB
- Reacts with: Human
- Isotype: IgG
Overview
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Product name
Anti-MT-ND5 antibody
See all MT-ND5 primary antibodies -
Description
Rabbit polyclonal to MT-ND5 -
Host species
Rabbit -
Tested applications
Suitable for: WBmore details -
Species reactivity
Reacts with: Human -
Immunogen
Synthetic peptide derived from an internal region of Human MT-ND5
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Positive control
- Jurkat cell lysate
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General notes
The Life Science industry has been in the grips of a reproducibility crisis for a number of years. Abcam is leading the way in addressing this with our range of recombinant monoclonal antibodies and knockout edited cell lines for gold-standard validation. Please check that this product meets your needs before purchasing.
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Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Store at -20ºC. -
Storage buffer
pH: 7.40
Preservative: 0.02% Sodium azide
Constituents: 49% PBS, 0.88% Sodium chloride, 50% Glycerol (glycerin, glycerine)
PBS is without Mg2+ and Ca2+ -
Concentration information loading...
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Purity
Immunogen affinity purified -
Purification notes
ab138136 was affinity purified from rabbit antiserum by immunogenic peptide affinity chromatography. -
Clonality
Polyclonal -
Isotype
IgG -
Research areas
Associated products
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Compatible Secondaries
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Isotype control
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Positive Controls
Applications
The Abpromise guarantee
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.
Application | Abreviews | Notes |
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WB |
1/500 - 1/1000. Predicted molecular weight: 67 kDa.
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Notes |
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WB
1/500 - 1/1000. Predicted molecular weight: 67 kDa. |
Target
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Function
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. -
Involvement in disease
Defects 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 similarities
Belongs to the complex I subunit 5 family. -
Cellular localization
Mitochondrion inner membrane. - Information by UniProt
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Database links
- Entrez Gene: 4540 Human
- Omim: 516005 Human
- SwissProt: P03915 Human
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Alternative names
- Complex I, subunit ND5 antibody
- EC 1.6.5.3 antibody
- Mitochondrially encoded NADH dehydrogenase 5 antibody
see all
Images
Datasheets and documents
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SDS download
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Datasheet download
References (1)
ab138136 has been referenced in 1 publication.
- Ji Y et al. Complex I mutations synergize to worsen the phenotypic expression of Leber's hereditary optic neuropathy. J Biol Chem 295:13224-13238 (2020). PubMed: 32723871