Component

Decaprenyl diphosphate

Decaprenyl diphosphate. Species, exposure and limitations are retained in each linked claim.

2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

Where it participates (unsigned role)

  1. A homozygous COQ2 variant caused severe impairment of CoQ10 synthesis in patient fibroblasts.

    Human 4-hydroxybenzoate polyprenyltransferase / COQ2 → Coenzyme Q biosynthesis source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/coq10-research/16400613.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bd16a213ac563cf32b275cdee32ba3082e6c296cf9129e0930e2f96f0d2dc72a", "start_char": 0, "end_char": 1000, "text_sha256": "bd16a213ac563cf32b275cdee32ba3082e6c296cf9129e0930e2f96f0d2dc72a"}
    experimental_model
    Family sequencing and fibroblast tracer assays
    exposure
    Homozygous COQ2 missense variant
    limitations
    Rare primary deficiency; sequence numbering follows the original publication.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    Human siblings
    plain_language
    Having the building blocks does not help if the enzyme that joins them is defective.
    primary_references
    [coq10-p16400613] A mutation in para-hydroxybenzoate-polyprenyl transferase (COQ2) causes primary coenzyme Q10 deficiency. (2006). https://pubmed.ncbi.nlm.nih.gov/16400613/ DOI: 10.1086/500092
    tissue_or_cell_type
    CoQ synthesis
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 229–240

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Family sequencing and fibroblast tracer assays · source_derived_draft · unverified_draft

    ### coq10-coq2-loss A homozygous COQ2 variant caused severe impairment of CoQ10 synthesis in patient fibroblasts. Condition category: machinery_impairment nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Having the building blocks does not help if the enzyme that joins them is defective. organism: Human siblings tissue_or_cell_type: CoQ synthesis experimental_model: Family sequencing and fibroblast tracer assays limitations: Rare primary deficiency; sequence numbering follows the original publication. exposure: Homozygous COQ2 missense variant evidence_span: {"source_cache": "artifacts/coq10-research/16400613.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "bd16a213ac563cf32b275cdee32ba3082e6c296cf9129e0930e2f96f0d2dc72a", "start_char": 0, "end_char": 1000, "text_sha256": "bd16a213ac563cf32b275cdee32ba3082e6c296cf9129e0930e2f96f0d2dc72a"} [coq10-p16400613] A mutation in para-hydroxybenzoate-polyprenyl transferase (COQ2) causes primary coenzyme Q10 deficiency. (2006). https://pubmed.ncbi.nlm.nih.gov/16400613/ DOI: 10.1086/500092
    Complete structured claim and evidence

  2. Patient fibroblasts with PDSS2 variants had severely impaired decaprenyl-diphosphate synthesis.

    Human decaprenyl-diphosphate synthase subunit 2 / PDSS2 → Coenzyme Q isoprenoid side-chain biosynthesis source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/coq10-research/17186472.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e9c50c316029827591ba4c9e6cc96b6a1b7b890f5b8dadfd88ac686c73d83865", "start_char": 0, "end_char": 1039, "text_sha256": "e9c50c316029827591ba4c9e6cc96b6a1b7b890f5b8dadfd88ac686c73d83865"}
    experimental_model
    Human genetics and radiolabeled-substrate assays
    exposure
    Compound heterozygous PDSS2 variants
    limitations
    Rare genetic disease; dietary shortage and tissue-wide thresholds were not established.
    nutrient_topic
    Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
    organism
    Human infant and patient fibroblasts
    plain_language
    The cell cannot finish CoQ normally if its tail-building machinery is impaired.
    primary_references
    [coq10-p17186472] Leigh syndrome with nephropathy and CoQ10 deficiency due to decaprenyl diphosphate synthase subunit 2 (PDSS2) mutations. (2006). https://pubmed.ncbi.nlm.nih.gov/17186472/ DOI: 10.1086/510023
    tissue_or_cell_type
    Muscle and fibroblast CoQ production
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 190–201

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human genetics and radiolabeled-substrate assays · source_derived_draft · unverified_draft

    ### coq10-pdss2 Patient fibroblasts with PDSS2 variants had severely impaired decaprenyl-diphosphate synthesis. Condition category: machinery_impairment nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cell cannot finish CoQ normally if its tail-building machinery is impaired. organism: Human infant and patient fibroblasts tissue_or_cell_type: Muscle and fibroblast CoQ production experimental_model: Human genetics and radiolabeled-substrate assays limitations: Rare genetic disease; dietary shortage and tissue-wide thresholds were not established. exposure: Compound heterozygous PDSS2 variants evidence_span: {"source_cache": "artifacts/coq10-research/17186472.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e9c50c316029827591ba4c9e6cc96b6a1b7b890f5b8dadfd88ac686c73d83865", "start_char": 0, "end_char": 1039, "text_sha256": "e9c50c316029827591ba4c9e6cc96b6a1b7b890f5b8dadfd88ac686c73d83865"} [coq10-p17186472] Leigh syndrome with nephropathy and CoQ10 deficiency due to decaprenyl diphosphate synthase subunit 2 (PDSS2) mutations. (2006). https://pubmed.ncbi.nlm.nih.gov/17186472/ DOI: 10.1086/510023
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards