Pathway candidateNCBI-verifiedprotein-coding

MT-ATP6

ATP synthase F0 subunit 6

NCBI Gene: 4508 GeneCards UniProt: P00846

Pathway candidate — not linked to PFS or PSSD by any record here

MT-ATP6 is in the library because it belongs to the mitochondria & energy family. No study, report or commentary in the corpus names it, so a variant in MT-ATP6 is not, by itself, evidence of anything related to post-drug syndromes.

Gene summary

A protein-coding gene on chromosome MT (mitochondrial) (mitochondrial function and energy). Enables proton channel activity. Contributes to proton-transporting ATP synthase activity, rotational mechanism.

Source: NCBI Gene, accessed 2026-10-07.

Protein reference (UniProt)

Protein: ATP synthase F(0) complex subunit a
Function (excerpt): Subunit a, of the mitochondrial membrane ATP synthase complex (F(1)F(0) ATP synthase or Complex V) that produces ATP from ADP in the presence of a proton gradient across the membrane which is generated by electron transport complexes of the respiratory chain (Probable). ATP synthase complex consist of a soluble F(1) head domain - the catalytic core - and a membrane F(1) domain - the membrane proton channel. These two domains are linked by a central stalk rotating inside the F(1) region and a stationary peripheral stalk. During catalysis, ATP synthesis in the catalytic domain of F(1) is coupled via a rotary mechanism of the central stalk subunits to proton translocation (Probable). With the subunit c (ATP5MC1), forms the proton-conducting channel in the F(0) domain, that contains two crucial half-channels (inlet and outlet) that facilitate proton movement from the mitochondrial intermembrane space (IMS) into the matrix.
Subcellular location: Mitochondrion inner membrane.
Associated conditions: Neuropathy, ataxia, and retinitis pigmentosa (NARP); Leber hereditary optic neuropathy (LHON); Leigh syndrome (LS); Mitochondrial infantile bilateral striatal necrosis (MIBSN); Mitochondrial complex V deficiency, mitochondrial 1 (MC5DM1); Myopathy, lactic acidosis, and sideroblastic anemia 3 (MLASA3); Ataxia and polyneuropathy, adult-onset (APAO); Cardiomyopathy, infantile hypertrophic (CMHI).

Source: UniProtKB/Swiss-Prot P00846, release 2026_03, licensed CC BY 4.0. This is the protein’s normal biology, not evidence about post-drug syndromes; associated conditions are inherited disorders of the gene, not PFS, PSSD or PRSD.

Why its pathway is in the library

Mitochondrial dysfunction and oxidative stress are reported in PFS/PSSD patient work; energy failure plausibly contributes to fatigue, cognitive, and sexual symptoms.

Written for the whole mitochondria & energy family, not for MT-ATP6 specifically.

Mentioned in 0 corpus records

No corpus record names MT-ATP6 directly yet. It is in the library because it sits in a pathway the corpus tracks (Mitochondria & energy).

Also in mitochondrial function and energy

All 33 genes

Browse by family on the gene families page.

Protein reference (UniProt)

Protein: ATP synthase F(0) complex subunit a
Function (excerpt): Subunit a, of the mitochondrial membrane ATP synthase complex (F(1)F(0) ATP synthase or Complex V) that produces ATP from ADP in the presence of a proton gradient across the membrane which is generated by electron transport complexes of the respiratory chain (Probable). ATP synthase complex consist of a soluble F(1) head domain - the catalytic core - and a membrane F(1) domain - the membrane proton channel. These two domains are linked by a central stalk rotating inside the F(1) region and a stationary peripheral stalk. During catalysis, ATP synthesis in the catalytic domain of F(1) is coupled via a rotary mechanism of the central stalk subunits to proton translocation (Probable). With the subunit c (ATP5MC1), forms the proton-conducting channel in the F(0) domain, that contains two crucial half-channels (inlet and outlet) that facilitate proton movement from the mitochondrial intermembrane space (IMS) into the matrix.
Subcellular location: Mitochondrion inner membrane.
Associated conditions: Neuropathy, ataxia, and retinitis pigmentosa (NARP); Leber hereditary optic neuropathy (LHON); Leigh syndrome (LS); Mitochondrial infantile bilateral striatal necrosis (MIBSN); Mitochondrial complex V deficiency, mitochondrial 1 (MC5DM1); Myopathy, lactic acidosis, and sideroblastic anemia 3 (MLASA3); Ataxia and polyneuropathy, adult-onset (APAO); Cardiomyopathy, infantile hypertrophic (CMHI).