Target intelligence / Profile preview

Formation of mitochondrial complex V assembly factor 1 homolog (FMC1)

Target
FMC1
Molecular classification
Other (Mitochondrial assembly factor; not enzyme, receptor, transporter, channel, or TF)
01

Overview

Formation of mitochondrial complex V assembly factor 1 homolog (FMC1) is a mitochondrial protein-coding gene and protein that acts as an assembly/stability factor for ATP synthase (complex V) within the mitochondrion inner membrane. FMC1 does not have catalytic activity but is required for proper assembly and stability of F(1)F(0) ATP synthase, which is essential for oxidative phosphorylation and cellular energy production. Pathogenic variants or dysfunction in FMC1 can impair ATP synthase assembly, potentially leading to mitochondrial pathologies such as Leigh disease and other OXPHOS disorders. While FMC1 is crucial for energy metabolism, it is not currently a therapeutic drug target, and no drugs are reported to modulate its activity directly. Note: - FMC1 is not a receptor, enzyme, transporter, ion channel, or commonly drugged target but falls under "other" as a mitochondrial assembly factor. - There are currently no known drugs interacting directly with FMC1, nor established pharmacological mechanisms or clinical biomarkers using FMC1 status. - Its disease roles are based on rare genetic disorders and research associations rather than large-scale clinical evidence.

Other names
Protein FMC1 homologFMC1C7orf55HSPC268ATP synthase assembly factor FMC1 (mitochondrial)UPF0562 protein C7orf55formation of mitochondrial complexes 1 homolog (S. cerevisiae)
02

Biological functions

Mitochondrial ATP synthase (complex V) assemblystability of ATP synthasemitochondrial proton-transporting ATP synthase complex assembly
03

Disease associations

Mitochondrial disease (including possible roles in Leigh disease and Usher syndrome based on gene association)Ovarian cancer
04

Safety considerations

Loss or dysfunction may compromise ATP synthesis and mitochondrial function, possibly leading to mitochondrial disease

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