• Product name

  • Description

    Rabbit polyclonal to MT-ND5
  • Host species

  • Tested applications

    Suitable for: IHC-P, WB, Flow Cytmore details
  • Species reactivity

    Reacts with: Human
  • Immunogen

    Recombinant full length protein corresponding to Human MT-ND5 aa 544-570 (C terminal) conjugated to keyhole limpet haemocyanin.


    Database link: P03915

  • Positive control

    • IHC-P: Human skeletal muscle tissue. WB: CRRF-CEM whole cell lysate. Flow: CRRF-CEM cells.



Our Abpromise guarantee covers the use of ab230509 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
IHC-P 1/50 - 1/100.
WB 1/1000. Predicted molecular weight: 67 kDa.
Flow Cyt 1/10 - 1/50.


  • 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
  • Database links

  • Alternative names

    • Complex I, subunit ND5 antibody
    • EC antibody
    • Mitochondrially encoded NADH dehydrogenase 5 antibody
    • MT ND5 antibody
    • MT-ND5 antibody
    • MTND 5 antibody
    • MTND5 antibody
    • NAD5 antibody
    • NADH dehydrogenase subunit 5 (complex I) antibody
    • NADH dehydrogenase subunit 5 antibody
    • NADH ubiquinone oxidoreductase , subunit ND5 antibody
    • NADH ubiquinone oxidoreductase chain 5 antibody
    • NADH-ubiquinone oxidoreductase chain 5 antibody
    • NADH5 antibody
    • ND5 antibody
    • NU5M_HUMAN antibody
    see all


  • Anti-MT-ND5 antibody (ab230509) at 1/1000 dilution + CRRF-CEM (Human T cell lymphoblast cell line) whole cell lysate at 1/35 dilution

    Predicted band size: 67 kDa

  • Flow cytometric analysis of CRRF-CEM (human T cell lymphoblast cell line) labelling MT-ND5 using ab230509 at 1/10 dilution (bottom histogram) compared to the negetive control (top histogram). FITC-conjugated goat-anti-rabbit secondary antibodies were used for the analysis.

  • Formalin-fixed, paraffin-embedded human skeletal tissue stained for MT-ND5 using ab230509 at 1/50 dilution in immunhistochemical analysis.


ab230509 has not yet been referenced specifically in any publications.

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