NDUFV1 Antibody | 60-532

NDUFV1 Antibody | 60-532 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human

Homology: Predicted species reactivity based on immunogen sequence: Bovine, Monkey, Mouse

Immunogen: This NDUFV1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 21-50 amino acids from the N-terminal region of human NDUFV1.

Research Area: Cancer, Obesity, Signal Transduction

Tested Application: WB

Application: For WB starting dilution is: 1:1000

Specificiy: N/A

Positive Control 1: N/A

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: 51 kDa

Validation: N/A

Isoform: N/A

Purification: This antibody is purified through a protein A column, followed by peptide affinity purification.

Clonality: Polyclonal

Clone: N/A

Isotype: Rabbit Ig

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.

Concentration: batch dependent

Storage Condition: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

Alternate Name: NADH dehydrogenase [ubiquinone] flavoprotein 1, mitochondrial, Complex I-51kD, CI-51kD, NADH dehydrogenase flavoprotein 1, NADH-ubiquinone oxidoreductase 51 kDa subunit, NDUFV1, UQOR1

User Note: Optimal dilutions for each application to be determined by the researcher.

BACKGROUND: The mitochondrial respiratory chain provides energy to cells via oxidative phosphorylation and consists of four membrane-bound electron-transporting protein complexes (I-IV) and an ATP synthase (complex V) . This gene encodes a 51 kDa subunit of the NADH:ubiquinone oxidoreductase complex I; a large complex with at least 45 nuclear and mitochondrial encoded subunits that liberates electrons from NADH and channels them to ubiquinone. This subunit carries the NADH-binding site as well as flavin mononucleotide (FMN) - and Fe-S-biding sites. Defects in complex I are a common cause of mitochondrial dysfunction; a syndrome that occurs in approximately 1 in 10, 000 live births. Mitochondrial complex I deficiency is linked to myopathies, encephalomyopathies, and neurodegenerative disorders such as Parkinson's disease and Leigh syndrome. Alternative splicing results in multiple transcript variants encoding distinct isoforms.