Pathway candidateNCBI-verifiedprotein-coding

ATP5F1A

ATP synthase F1 subunit alpha

NCBI Gene: 498 Ensembl GeneCards UniProt: P25705

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

ATP5F1A 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 ATP5F1A is not, by itself, evidence of anything related to post-drug syndromes.

Gene summary

A protein-coding gene on chromosome 18 (mitochondrial function and energy). Encodes a subunit of mitochondrial ATP synthase. Mitochondrial ATP synthase catalyzes ATP synthesis, using an electrochemical gradient of protons across the inner membrane during oxidative phosphorylation.

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

Protein reference (UniProt)

Protein: ATP synthase F(1) complex subunit alpha, mitochondrial
Function (excerpt): Subunit alpha, 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). In vivo, can only synthesize ATP although its ATP hydrolase activity can be activated artificially in vitro (By similarity). With the catalytic subunit beta (ATP5F1B), forms the catalytic core in the F(1) domain. Subunit alpha does not bear the catalytic high-affinity ATP-binding sites (Probable).
Subcellular location: Mitochondrion; Mitochondrion inner membrane; Cell membrane.
Tissue specificity: Fetal lung, heart, liver, gut and kidney. Expressed at higher levels in the fetal brain, retina and spinal cord.
Associated conditions: Combined oxidative phosphorylation deficiency 22 (COXPD22); Mitochondrial complex V deficiency, nuclear type 4A (MC5DN4A); Mitochondrial complex V deficiency, nuclear type 4B (MC5DN4B).

Source: UniProtKB/Swiss-Prot P25705, 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 ATP5F1A specifically.

Mentioned in 0 corpus records

No corpus record names ATP5F1A 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

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Gene summary

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

Protein reference (UniProt)

Protein: ATP synthase F(1) complex subunit alpha, mitochondrial
Function (excerpt): Subunit alpha, 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). In vivo, can only synthesize ATP although its ATP hydrolase activity can be activated artificially in vitro (By similarity). With the catalytic subunit beta (ATP5F1B), forms the catalytic core in the F(1) domain. Subunit alpha does not bear the catalytic high-affinity ATP-binding sites (Probable).
Subcellular location: Mitochondrion; Mitochondrion inner membrane; Cell membrane.
Tissue specificity: Fetal lung, heart, liver, gut and kidney. Expressed at higher levels in the fetal brain, retina and spinal cord.
Associated conditions: Combined oxidative phosphorylation deficiency 22 (COXPD22); Mitochondrial complex V deficiency, nuclear type 4A (MC5DN4A); Mitochondrial complex V deficiency, nuclear type 4B (MC5DN4B).