Component
Human colonic epithelial biotin uptake
Human colonic epithelial biotin uptake. 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 acts on it
Pantothenic acid competitively inhibited biotin uptake in NCM460 cells, with Ki 14.4 micromolar.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"}
- experimental_model
- Transport and inhibitor experiments in human NCM460 colonic epithelial cells
- exposure
- Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators
- limitations
- Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes.
- nutrient_topic
- Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
- organism
- Homo sapiens
- plain_language
- B5 and biotin can compete for entry in this colon-cell assay.
- primary_references
- [b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365
- tissue_or_cell_type
- Colonic epithelium; NCM460 culture
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 195–206
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transport and inhibitor experiments in human NCM460 colonic epithelial cells · source_derived_draft · unverified_draft
### b7-colon-b5-competition Pantothenic acid competitively inhibited biotin uptake in NCM460 cells, with Ki 14.4 micromolar. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: B5 and biotin can compete for entry in this colon-cell assay. organism: Homo sapiens tissue_or_cell_type: Colonic epithelium; NCM460 culture experimental_model: Transport and inhibitor experiments in human NCM460 colonic epithelial cells limitations: Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes. exposure: Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators evidence_span: {"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"} [b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365
Complete structured claim and evidencePKC activators reduced biotin uptake in NCM460 cells; PKC inhibitors modestly increased uptake.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"}
- experimental_model
- Transport and inhibitor experiments in human NCM460 colonic epithelial cells
- exposure
- Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators
- limitations
- Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes.
- nutrient_topic
- Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
- organism
- Homo sapiens
- plain_language
- Cell signaling changes how quickly colon cells admit biotin.
- primary_references
- [b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365
- tissue_or_cell_type
- Colonic epithelium; NCM460 culture
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 208–219
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transport and inhibitor experiments in human NCM460 colonic epithelial cells · source_derived_draft · unverified_draft
### b7-colon-pkc PKC activators reduced biotin uptake in NCM460 cells; PKC inhibitors modestly increased uptake. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cell signaling changes how quickly colon cells admit biotin. organism: Homo sapiens tissue_or_cell_type: Colonic epithelium; NCM460 culture experimental_model: Transport and inhibitor experiments in human NCM460 colonic epithelial cells limitations: Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes. exposure: Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators evidence_span: {"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"} [b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365
Complete structured claim and evidenceBiotin uptake in human NCM460 cells was saturable, energy dependent and sodium dependent, with apparent Km 19.7 micromolar.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"}
- experimental_model
- Transport and inhibitor experiments in human NCM460 colonic epithelial cells
- exposure
- Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators
- limitations
- Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes.
- nutrient_topic
- Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
- organism
- Homo sapiens
- plain_language
- Colon cells can take up free biotin through a saturable transport process.
- primary_references
- [b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365
- tissue_or_cell_type
- Colonic epithelium; NCM460 culture
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 182–193
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transport and inhibitor experiments in human NCM460 colonic epithelial cells · source_derived_draft · unverified_draft
### b7-colon-sodium Biotin uptake in human NCM460 cells was saturable, energy dependent and sodium dependent, with apparent Km 19.7 micromolar. Condition category: normal nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Colon cells can take up free biotin through a saturable transport process. organism: Homo sapiens tissue_or_cell_type: Colonic epithelium; NCM460 culture experimental_model: Transport and inhibitor experiments in human NCM460 colonic epithelial cells limitations: Cell-line kinetics do not quantify microbiome contributions or demonstrate competition at ordinary dietary intakes. exposure: Radiolabeled biotin with sodium replacement, pantothenate and kinase modulators evidence_span: {"source_cache": "artifacts/biotin-research/9814986.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be", "start_char": 0, "end_char": 1676, "text_sha256": "7cc679e31b95ae919c15fadf0d56933d2ed8074664e11cd80a96e910181857be"} [b7-p9814986] Biotin uptake by human colonic epithelial NCM460 cells: a carrier-mediated process shared with pantothenic acid. (1998). https://pubmed.ncbi.nlm.nih.gov/9814986/ DOI: 10.1152/ajpcell.1998.275.5.c1365
Complete structured claim and evidenceLPS reduced carrier-mediated biotin uptake in NCM460 cells; CK2 inhibition and a putative CK2-site SMVT mutant supported a CK2-related trafficking mechanism.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/biotin-research/28052864.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f27f27a7730837eff6529a7eccf67b3587df28af01ac0507d1b692410483703", "start_char": 0, "end_char": 1549, "text_sha256": "2f27f27a7730837eff6529a7eccf67b3587df28af01ac0507d1b692410483703"}
- experimental_model
- LPS exposure of human NCM460 cells with separate mouse experiments
- exposure
- LPS, CK2 inhibitors and SMVT Thr78Ala mutation
- limitations
- CK2 involvement is supported experimentally but the full causal sequence remains qualified; whole-body human deficiency was not measured.
- nutrient_topic
- Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
- organism
- Homo sapiens
- plain_language
- Inflammatory exposure interfered with biotin entry in this model.
- primary_references
- [b7-p28052864] Lipopolysaccharide inhibits colonic biotin uptake via interference with membrane expression of its transporter: a role for a casein kinase 2-mediated pathway. (2017). https://pubmed.ncbi.nlm.nih.gov/28052864/ DOI: 10.1152/ajpcell.00300.2016
- tissue_or_cell_type
- Colonic epithelial NCM460 cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 1118–1129
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · LPS exposure of human NCM460 cells with separate mouse experiments · source_derived_draft · unverified_draft
### b7-lps-uptake LPS reduced carrier-mediated biotin uptake in NCM460 cells; CK2 inhibition and a putative CK2-site SMVT mutant supported a CK2-related trafficking mechanism. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Inflammatory exposure interfered with biotin entry in this model. organism: Homo sapiens tissue_or_cell_type: Colonic epithelial NCM460 cells experimental_model: LPS exposure of human NCM460 cells with separate mouse experiments limitations: CK2 involvement is supported experimentally but the full causal sequence remains qualified; whole-body human deficiency was not measured. exposure: LPS, CK2 inhibitors and SMVT Thr78Ala mutation evidence_span: {"source_cache": "artifacts/biotin-research/28052864.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2f27f27a7730837eff6529a7eccf67b3587df28af01ac0507d1b692410483703", "start_char": 0, "end_char": 1549, "text_sha256": "2f27f27a7730837eff6529a7eccf67b3587df28af01ac0507d1b692410483703"} [b7-p28052864] Lipopolysaccharide inhibits colonic biotin uptake via interference with membrane expression of its transporter: a role for a casein kinase 2-mediated pathway. (2017). https://pubmed.ncbi.nlm.nih.gov/28052864/ DOI: 10.1152/ajpcell.00300.2016
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.