Anti-MT-ND5 antibody (ab230772)
- Datasheet
- References
- Protocols
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: IHC-P, WBmore details -
Species reactivity
Reacts with: Human
Predicted to work with: Mouse, Rat -
Immunogen
Synthetic peptide corresponding to Human MT-ND5 aa 321-370.
Sequence:QPHLAFLHICTHAFFKAMLFMCSGSIIHNLNNEQDIRKMGGLLKTMPLTS
Database link: P03915 -
Positive control
- IHC-P: Human heart tissue. WB: HT-29 cells.
Properties
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Form
Liquid -
Storage instructions
Shipped 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 buffer
pH: 7.2
Preservative: 0.05% Sodium azide
Constituent: PBS -
Concentration information loading...
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Purity
Immunogen affinity purified -
Clonality
Polyclonal -
Isotype
IgG -
Research areas
Associated products
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Compatible Secondaries
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Isotype control
Applications
Our Abpromise guarantee covers the use of ab230772 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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IHC-P | 1/200. | |
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
- Entrez Gene: 17721 Mouse
- Entrez Gene: 26202 Rat
- Omim: 516005 Human
- SwissProt: P03915 Human
- SwissProt: P03921 Mouse
- SwissProt: P11661 Rat
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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
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Anti-MT-ND5 antibody (ab230772) at 1/500 dilution + HT-29 (human colorectal adenocarcinoma cell line) cell extract
Developed using the ECL technique.
Predicted band size: 67 kDa -
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-MT-ND5 antibody (ab230772)
Formalin-fixed, paraffin-embedded human heart tissue stained for MT-ND5 using ab230772 at 1/200 dilution in immunohistochemical analysis.
Datasheets and documents
References
ab230772 has not yet been referenced specifically in any publications.