Component
Mitochondrial thiamine diphosphate content
ThDP measured in isolated mitochondrial fractions.
2 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 acts on it
G177A patient lymphoblasts had approximately tenfold lower mitochondrial ThDP despite modestly increased cytosolic ThDP.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence-scope
- Patient lymphoblasts
- evidence_locator
- Table 1
- evidence_spans
- [{"source_document": "artifacts/thiamine_transport_sources/PMC1595310.txt", "start_char": 14675, "end_char": 15382}]
- experimental_model
- Human recombinant carrier, patient lymphoblasts and Slc25a19-null mouse embryonic fibroblasts.
- limitations
- Cultured lymphoblast fractions; not a plasma threshold.
- nutrient_topic
- Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
- organism
- Homo sapiens
- plain_language
- B1 cofactor can remain outside mitochondria when its carrier fails.
- primary_references
- [lindhurst-2006-slc25a19] Knockout of Slc25a19 causes mitochondrial thiamine pyrophosphate depletion, embryonic lethality, CNS malformations, and anemia (2006). https://pmc.ncbi.nlm.nih.gov/articles/PMC1595310/ DOI: 10.1073/pnas.0607661103
- tissue_or_cell_type
- Patient lymphoblasts
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 431–443
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human recombinant carrier, patient lymphoblasts and Slc25a19-null mouse embryonic fibroblasts. · source_derived_draft · unverified_draft
### b1-slc25a19-human-pool-separation G177A patient lymphoblasts had approximately tenfold lower mitochondrial ThDP despite modestly increased cytosolic ThDP. Condition category: machinery_impairment nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: B1 cofactor can remain outside mitochondria when its carrier fails. organism: Homo sapiens tissue_or_cell_type: Patient lymphoblasts experimental_model: Human recombinant carrier, patient lymphoblasts and Slc25a19-null mouse embryonic fibroblasts. limitations: Cultured lymphoblast fractions; not a plasma threshold. evidence_locator: Table 1 evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/PMC1595310.txt", "start_char": 14675, "end_char": 15382}] evidence-scope: Patient lymphoblasts [lindhurst-2006-slc25a19] Knockout of Slc25a19 causes mitochondrial thiamine pyrophosphate depletion, embryonic lethality, CNS malformations, and anemia (2006). https://pmc.ncbi.nlm.nih.gov/articles/PMC1595310/ DOI: 10.1073/pnas.0607661103
Complete structured claim and evidenceThDP was undetectable in knockout fibroblast mitochondrial fractions while cytosolic ThDP increased.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence-scope
- Embryonic fibroblasts
- evidence_locator
- Table 1
- evidence_spans
- [{"source_document": "artifacts/thiamine_transport_sources/PMC1595310.txt", "start_char": 14675, "end_char": 15382}]
- experimental_model
- Human recombinant carrier, patient lymphoblasts and Slc25a19-null mouse embryonic fibroblasts.
- limitations
- Undetectable means below this assay detection, not proven absolute zero.
- nutrient_topic
- Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
- organism
- Mus musculus
- plain_language
- Deleting the carrier separates cellular B1 supply from mitochondrial availability.
- primary_references
- [lindhurst-2006-slc25a19] Knockout of Slc25a19 causes mitochondrial thiamine pyrophosphate depletion, embryonic lethality, CNS malformations, and anemia (2006). https://pmc.ncbi.nlm.nih.gov/articles/PMC1595310/ DOI: 10.1073/pnas.0607661103
- tissue_or_cell_type
- Embryonic fibroblasts
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 445–457
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human recombinant carrier, patient lymphoblasts and Slc25a19-null mouse embryonic fibroblasts. · source_derived_draft · unverified_draft
### b1-slc25a19-mouse-mito-depletion ThDP was undetectable in knockout fibroblast mitochondrial fractions while cytosolic ThDP increased. Condition category: machinery_impairment nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Deleting the carrier separates cellular B1 supply from mitochondrial availability. organism: Mus musculus tissue_or_cell_type: Embryonic fibroblasts experimental_model: Human recombinant carrier, patient lymphoblasts and Slc25a19-null mouse embryonic fibroblasts. limitations: Undetectable means below this assay detection, not proven absolute zero. evidence_locator: Table 1 evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/PMC1595310.txt", "start_char": 14675, "end_char": 15382}] evidence-scope: Embryonic fibroblasts [lindhurst-2006-slc25a19] Knockout of Slc25a19 causes mitochondrial thiamine pyrophosphate depletion, embryonic lethality, CNS malformations, and anemia (2006). https://pmc.ncbi.nlm.nih.gov/articles/PMC1595310/ DOI: 10.1073/pnas.0607661103
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.