NU4LM rabbit pAb

Cat :A18628

Price: ¥900¥1600
Size: 50ul 100ul
  • Source

    Rabbit

  • Applications

    WB,ELISA

  • Reactivity

    Human

  • Dilution

    WB 1:500-2000 ELISA 1:5000-20000

  • Storage

    -20°C/1 year

  • Specificity

    NU4LM Polyclonal Antibody detects endogenous levels of protein.

  • Source/Purification

    The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.

  • Immunogen

    Synthesized peptide derived from human protein . at AA range: 10-90

  • Uniprot No

    P03901

  • Form

    Liquid in PBS containing 50% glycerol, and 0.02% sodium azide.

  • Clonality

    Polyclonal

  • Isotype

    IgG

  • Background

    catalytic activity:NADH + ubiquinone = NAD(+) + ubiquinol.,disease:Defects 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.,disease: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.,disease: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.,disease:Defects in MT-ND4L 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.,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.,similarity:Belongs to the complex I subunit 4 family.,similarity:Belongs to the complex I subunit 4L family.,

  • Other

    MT-ND4L MTND4L NADH4L ND4L, NADH-ubiquinone oxidoreductase chain 4L (EC 1.6.5.3) (NADH dehydrogenase subunit 4L)

  • Concentration

    1 mg/ml

Product Reactivity Applications Conjugation Catalog Images