Target intelligence / Profile preview

NADH dehydrogenase [ubiquinone] 1 beta subcomplex subunit 4 (NDUFB4)

Target
NDUFB4
Molecular classification
Enzyme accessory subunit (accessory subunit of mitochondrial NADH:ubiquinone oxidoreductase, Complex I), Mitochondrial electron transport chain protein
01

Overview

NADH dehydrogenase [ubiquinone] 1 beta subcomplex subunit 4 (NDUFB4) is an accessory, non-catalytic subunit of mitochondrial Complex I, the first and largest enzyme in the electron transport chain. Complex I is crucial for cellular energy production, mediating the transfer of electrons from NADH to ubiquinone[1][2][6][7]. NDUFB4 contributes to the structure and assembly of the complex but does not participate directly in redox catalysis. Mutations or loss of function in NDUFB4 have been associated with mitochondrial disease, implicating it in the integrity and functionality of mitochondrial respiration[2][6]. There are currently no drugs or approved therapies that selectively target NDUFB4, nor is it used as a biomarker in clinical practice.

Other names
NDUFB4NADH:ubiquinone oxidoreductase subunit B4NADH dehydrogenase [ubiquinone] 1 beta subcomplex subunit 4Complex I-B15CI-B15NADH-ubiquinone oxidoreductase B15 subunitB15Complex I B15 subunitNADH dehydrogenase (ubiquinone) 1 beta subcomplex, 4, 15kDa
02

Biological functions

Electron transport: participates as a structural and accessory subunit in mitochondrial Complex I, which transfers electrons from NADH to ubiquinone during cellular respirationMitochondrial respiration: helps maintain the integrity and function of Complex I in the oxidative phosphorylation pathwayComplex assembly/biogenesis: may contribute to scaffolding and assembly of complex I
03

Disease associations

Mitochondrial disease: variants or loss of function are associated with mitochondrial disordersPolyomavirus-associated nephropathy: linked in gene-disease databasesOther possible associations via dysfunction of mitochondrial complex I (implied)
04

Safety considerations

Dysfunction could potentially result in impaired mitochondrial respiration and associated toxicity, but no specific safety issues or therapeutic challenges have been documented for targeting NDUFB4 directly

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