Component
Human cytochrome c oxidase assembly factor COA6
Human cytochrome c oxidase assembly factor COA6. Species, exposure and limitations are retained in each linked claim.
4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
COA6 loss reduced membrane potential and impaired potential-dependent protein import across the inner mitochondrial membrane.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/copper-research/32061935.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a", "start_char": 0, "end_char": 1043, "text_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a"}
- experimental_model
- COA6 knockout HEK293T cells and biochemical protein interaction experiments
- exposure
- COA6 loss; SCO1/SCO2 disulfide reduction assays
- limitations
- COA6 machinery failure is not dietary copper depletion. Protein import effects were selective rather than universal loss of all mitochondrial import.
- nutrient_topic
- Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
- organism
- Human cells and proteins
- plain_language
- The energy deficit can interfere with importing other mitochondrial proteins.
- primary_references
- [copper-p32061935] COA6 Facilitates Cytochrome c Oxidase Biogenesis as Thiol-reductase for Copper Metallochaperones in Mitochondria. (2020). https://pubmed.ncbi.nlm.nih.gov/32061935/ DOI: 10.1016/j.jmb.2020.01.036
- tissue_or_cell_type
- Mitochondrial intermembrane space
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 689–700
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · COA6 knockout HEK293T cells and biochemical protein interaction experiments · source_derived_draft · unverified_draft
### copper-coa6-protein-import COA6 loss reduced membrane potential and impaired potential-dependent protein import across the inner mitochondrial membrane. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The energy deficit can interfere with importing other mitochondrial proteins. organism: Human cells and proteins tissue_or_cell_type: Mitochondrial intermembrane space experimental_model: COA6 knockout HEK293T cells and biochemical protein interaction experiments limitations: COA6 machinery failure is not dietary copper depletion. Protein import effects were selective rather than universal loss of all mitochondrial import. exposure: COA6 loss; SCO1/SCO2 disulfide reduction assays evidence_span: {"source_cache": "artifacts/copper-research/32061935.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a", "start_char": 0, "end_char": 1043, "text_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a"} [copper-p32061935] COA6 Facilitates Cytochrome c Oxidase Biogenesis as Thiol-reductase for Copper Metallochaperones in Mitochondria. (2020). https://pubmed.ncbi.nlm.nih.gov/32061935/ DOI: 10.1016/j.jmb.2020.01.036
Complete structured claim and evidenceCOA6 loss caused combined respiratory complex I and IV deficiency in human cells.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/copper-research/32061935.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a", "start_char": 0, "end_char": 1043, "text_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a"}
- experimental_model
- COA6 knockout HEK293T cells and biochemical protein interaction experiments
- exposure
- COA6 loss; SCO1/SCO2 disulfide reduction assays
- limitations
- COA6 machinery failure is not dietary copper depletion. Protein import effects were selective rather than universal loss of all mitochondrial import.
- nutrient_topic
- Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
- organism
- Human cells and proteins
- plain_language
- A failure in copper-enzyme assembly can affect more than one respiratory complex.
- primary_references
- [copper-p32061935] COA6 Facilitates Cytochrome c Oxidase Biogenesis as Thiol-reductase for Copper Metallochaperones in Mitochondria. (2020). https://pubmed.ncbi.nlm.nih.gov/32061935/ DOI: 10.1016/j.jmb.2020.01.036
- tissue_or_cell_type
- Mitochondrial intermembrane space
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 676–687
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · COA6 knockout HEK293T cells and biochemical protein interaction experiments · source_derived_draft · unverified_draft
### copper-coa6-respiratory-loss COA6 loss caused combined respiratory complex I and IV deficiency in human cells. Condition category: machinery_impairment nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: A failure in copper-enzyme assembly can affect more than one respiratory complex. organism: Human cells and proteins tissue_or_cell_type: Mitochondrial intermembrane space experimental_model: COA6 knockout HEK293T cells and biochemical protein interaction experiments limitations: COA6 machinery failure is not dietary copper depletion. Protein import effects were selective rather than universal loss of all mitochondrial import. exposure: COA6 loss; SCO1/SCO2 disulfide reduction assays evidence_span: {"source_cache": "artifacts/copper-research/32061935.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a", "start_char": 0, "end_char": 1043, "text_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a"} [copper-p32061935] COA6 Facilitates Cytochrome c Oxidase Biogenesis as Thiol-reductase for Copper Metallochaperones in Mitochondria. (2020). https://pubmed.ncbi.nlm.nih.gov/32061935/ DOI: 10.1016/j.jmb.2020.01.036
Complete structured claim and evidenceCOA6 acted as a thiol reductase for critical cysteine disulfides in SCO1.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/copper-research/32061935.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a", "start_char": 0, "end_char": 1043, "text_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a"}
- experimental_model
- COA6 knockout HEK293T cells and biochemical protein interaction experiments
- exposure
- COA6 loss; SCO1/SCO2 disulfide reduction assays
- limitations
- COA6 machinery failure is not dietary copper depletion. Protein import effects were selective rather than universal loss of all mitochondrial import.
- nutrient_topic
- Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
- organism
- Human cells and proteins
- plain_language
- An assembly factor prepares copper-binding sites for use.
- primary_references
- [copper-p32061935] COA6 Facilitates Cytochrome c Oxidase Biogenesis as Thiol-reductase for Copper Metallochaperones in Mitochondria. (2020). https://pubmed.ncbi.nlm.nih.gov/32061935/ DOI: 10.1016/j.jmb.2020.01.036
- tissue_or_cell_type
- Mitochondrial intermembrane space
Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 650–661
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · COA6 knockout HEK293T cells and biochemical protein interaction experiments · source_derived_draft · unverified_draft
### copper-coa6-sco1-reduction COA6 acted as a thiol reductase for critical cysteine disulfides in SCO1. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: An assembly factor prepares copper-binding sites for use. organism: Human cells and proteins tissue_or_cell_type: Mitochondrial intermembrane space experimental_model: COA6 knockout HEK293T cells and biochemical protein interaction experiments limitations: COA6 machinery failure is not dietary copper depletion. Protein import effects were selective rather than universal loss of all mitochondrial import. exposure: COA6 loss; SCO1/SCO2 disulfide reduction assays evidence_span: {"source_cache": "artifacts/copper-research/32061935.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a", "start_char": 0, "end_char": 1043, "text_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a"} [copper-p32061935] COA6 Facilitates Cytochrome c Oxidase Biogenesis as Thiol-reductase for Copper Metallochaperones in Mitochondria. (2020). https://pubmed.ncbi.nlm.nih.gov/32061935/ DOI: 10.1016/j.jmb.2020.01.036
Complete structured claim and evidenceCOA6 reduced critical SCO2 disulfides; SCO2 cysteines in its CX3CXnH domain mediated COA6 interaction.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/copper-research/32061935.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a", "start_char": 0, "end_char": 1043, "text_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a"}
- experimental_model
- COA6 knockout HEK293T cells and biochemical protein interaction experiments
- exposure
- COA6 loss; SCO1/SCO2 disulfide reduction assays
- limitations
- COA6 machinery failure is not dietary copper depletion. Protein import effects were selective rather than universal loss of all mitochondrial import.
- nutrient_topic
- Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
- organism
- Human cells and proteins
- plain_language
- The same assembly factor also prepares a second copper-handling protein.
- primary_references
- [copper-p32061935] COA6 Facilitates Cytochrome c Oxidase Biogenesis as Thiol-reductase for Copper Metallochaperones in Mitochondria. (2020). https://pubmed.ncbi.nlm.nih.gov/32061935/ DOI: 10.1016/j.jmb.2020.01.036
- tissue_or_cell_type
- Mitochondrial intermembrane space
Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 663–674
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · COA6 knockout HEK293T cells and biochemical protein interaction experiments · source_derived_draft · unverified_draft
### copper-coa6-sco2-reduction COA6 reduced critical SCO2 disulfides; SCO2 cysteines in its CX3CXnH domain mediated COA6 interaction. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same assembly factor also prepares a second copper-handling protein. organism: Human cells and proteins tissue_or_cell_type: Mitochondrial intermembrane space experimental_model: COA6 knockout HEK293T cells and biochemical protein interaction experiments limitations: COA6 machinery failure is not dietary copper depletion. Protein import effects were selective rather than universal loss of all mitochondrial import. exposure: COA6 loss; SCO1/SCO2 disulfide reduction assays evidence_span: {"source_cache": "artifacts/copper-research/32061935.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a", "start_char": 0, "end_char": 1043, "text_sha256": "7a7828c0b3a9e17878ed230d32af9dd51b667cd1ef0c934fb299f15b5a5e2b0a"} [copper-p32061935] COA6 Facilitates Cytochrome c Oxidase Biogenesis as Thiol-reductase for Copper Metallochaperones in Mitochondria. (2020). https://pubmed.ncbi.nlm.nih.gov/32061935/ DOI: 10.1016/j.jmb.2020.01.036
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.