Component
Mouse creatine transporter / Slc6a8
Mouse creatine transporter / Slc6a8. Species, exposure and limitations are retained in each linked claim.
5 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
Loss of Slc6a8 impaired CD8 T-cell antitumor immunity in the studied mouse models.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/creatine-research/31628186.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2547f09774244dc13d8bd95950b9b313b7fa625436ab778bb52913a64f2ae458", "start_char": 0, "end_char": 1076, "text_sha256": "2547f09774244dc13d8bd95950b9b313b7fa625436ab778bb52913a64f2ae458"}
- experimental_model
- Transporter-deficient T cells, tumor models and supplementation experiments
- exposure
- Slc6a8 deletion; creatine administration with or without checkpoint blockade
- limitations
- Preclinical tumor immunity; no human cancer efficacy or universal tumor effect is inferred.
- nutrient_topic
- Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
- organism
- Mice
- plain_language
- Having creatine available outside cells did not replace the missing transporter.
- primary_references
- [creatine-p31628186] Creatine uptake regulates CD8 T cell antitumor immunity. (2019). https://pubmed.ncbi.nlm.nih.gov/31628186/ DOI: 10.1084/jem.20182044
- tissue_or_cell_type
- CD8 T cells and transplanted tumor models
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 581–592
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter-deficient T cells, tumor models and supplementation experiments · source_derived_draft · unverified_draft
### creatine-tumor-transporter-loss Loss of Slc6a8 impaired CD8 T-cell antitumor immunity in the studied mouse models. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Having creatine available outside cells did not replace the missing transporter. organism: Mice tissue_or_cell_type: CD8 T cells and transplanted tumor models experimental_model: Transporter-deficient T cells, tumor models and supplementation experiments limitations: Preclinical tumor immunity; no human cancer efficacy or universal tumor effect is inferred. exposure: Slc6a8 deletion; creatine administration with or without checkpoint blockade evidence_span: {"source_cache": "artifacts/creatine-research/31628186.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2547f09774244dc13d8bd95950b9b313b7fa625436ab778bb52913a64f2ae458", "start_char": 0, "end_char": 1076, "text_sha256": "2547f09774244dc13d8bd95950b9b313b7fa625436ab778bb52913a64f2ae458"} [creatine-p31628186] Creatine uptake regulates CD8 T cell antitumor immunity. (2019). https://pubmed.ncbi.nlm.nih.gov/31628186/ DOI: 10.1084/jem.20182044
Complete structured claim and evidence
Where it participates (unsigned role)
CRT loss impaired epithelial barrier formation and wound healing; transporter-deficient organoids also had reduced barrier function.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/creatine-research/32433978.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1733708b77e75d099fa25665b9b9a9aa0af72143c985b6f0f2b931fb8f4c0887", "start_char": 0, "end_char": 2283, "text_sha256": "1733708b77e75d099fa25665b9b9a9aa0af72143c985b6f0f2b931fb8f4c0887"}
- experimental_model
- Transporter manipulation, intestinal organoids and human biopsy comparison
- exposure
- CRT knockdown/overexpression; transporter-deficient organoids; 30 Crohn disease, 27 ulcerative colitis and 30 control biopsies
- limitations
- Causal epithelial experiments and observational human expression findings are distinct; no human creatine treatment outcome was tested.
- nutrient_topic
- Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
- organism
- Human T84 cells, mouse organoids and human IBD biopsies
- plain_language
- Intestinal cells needed the transporter to maintain their barrier in these experiments.
- primary_references
- [creatine-p32433978] Creatine Transporter, Reduced in Colon Tissues From Patients With Inflammatory Bowel Diseases, Regulates Energy Balance in Intestinal Epithelial Cells, Epithelial Integrity, and Barrier Function. (2020). https://pubmed.ncbi.nlm.nih.gov/32433978/ DOI: 10.1053/j.gastro.2020.05.033
- tissue_or_cell_type
- Intestinal epithelium and tight junctions
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 646–657
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter manipulation, intestinal organoids and human biopsy comparison · source_derived_draft · unverified_draft
### creatine-gut-transporter-barrier CRT loss impaired epithelial barrier formation and wound healing; transporter-deficient organoids also had reduced barrier function. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Intestinal cells needed the transporter to maintain their barrier in these experiments. organism: Human T84 cells, mouse organoids and human IBD biopsies tissue_or_cell_type: Intestinal epithelium and tight junctions experimental_model: Transporter manipulation, intestinal organoids and human biopsy comparison limitations: Causal epithelial experiments and observational human expression findings are distinct; no human creatine treatment outcome was tested. exposure: CRT knockdown/overexpression; transporter-deficient organoids; 30 Crohn disease, 27 ulcerative colitis and 30 control biopsies evidence_span: {"source_cache": "artifacts/creatine-research/32433978.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1733708b77e75d099fa25665b9b9a9aa0af72143c985b6f0f2b931fb8f4c0887", "start_char": 0, "end_char": 2283, "text_sha256": "1733708b77e75d099fa25665b9b9a9aa0af72143c985b6f0f2b931fb8f4c0887"} [creatine-p32433978] Creatine Transporter, Reduced in Colon Tissues From Patients With Inflammatory Bowel Diseases, Regulates Energy Balance in Intestinal Epithelial Cells, Epithelial Integrity, and Barrier Function. (2020). https://pubmed.ncbi.nlm.nih.gov/32433978/ DOI: 10.1053/j.gastro.2020.05.033
Complete structured claim and evidenceCkb or Slc6a8 loss impaired T-cell function without changing global adenylate energy charge in the study.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/creatine-research/35235777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958", "start_char": 0, "end_char": 1025, "text_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958"}
- experimental_model
- Transporter or kinase loss, T-cell homeostasis and infection experiments
- exposure
- Slc6a8 or Ckb deletion
- limitations
- The study distinguishes TCR–mTORC1 signaling from whole-cell adenylate energy charge; it does not demonstrate clinical immune benefits of supplements.
- nutrient_topic
- Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
- organism
- Mice
- plain_language
- The observed signaling defect could not be reduced to a simple fall in the cell-wide energy measurement.
- primary_references
- [creatine-p35235777] Creatine transport and creatine kinase activity is required for CD8+ T cell immunity. (2022). https://pubmed.ncbi.nlm.nih.gov/35235777/ DOI: 10.1016/j.celrep.2022.110446
- tissue_or_cell_type
- Naive and activated CD8 T cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 633–644
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter or kinase loss, T-cell homeostasis and infection experiments · source_derived_draft · unverified_draft
### creatine-tcell-energy-charge Ckb or Slc6a8 loss impaired T-cell function without changing global adenylate energy charge in the study. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The observed signaling defect could not be reduced to a simple fall in the cell-wide energy measurement. organism: Mice tissue_or_cell_type: Naive and activated CD8 T cells experimental_model: Transporter or kinase loss, T-cell homeostasis and infection experiments limitations: The study distinguishes TCR–mTORC1 signaling from whole-cell adenylate energy charge; it does not demonstrate clinical immune benefits of supplements. exposure: Slc6a8 or Ckb deletion evidence_span: {"source_cache": "artifacts/creatine-research/35235777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958", "start_char": 0, "end_char": 1025, "text_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958"} [creatine-p35235777] Creatine transport and creatine kinase activity is required for CD8+ T cell immunity. (2022). https://pubmed.ncbi.nlm.nih.gov/35235777/ DOI: 10.1016/j.celrep.2022.110446
Complete structured claim and evidenceLoss of either Ckb or Slc6a8 compromised CD8 T-cell expansion in response to infection.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/creatine-research/35235777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958", "start_char": 0, "end_char": 1025, "text_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958"}
- experimental_model
- Transporter or kinase loss, T-cell homeostasis and infection experiments
- exposure
- Slc6a8 or Ckb deletion
- limitations
- The study distinguishes TCR–mTORC1 signaling from whole-cell adenylate energy charge; it does not demonstrate clinical immune benefits of supplements.
- nutrient_topic
- Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
- organism
- Mice
- plain_language
- Both the transporter and the phosphate-transfer enzyme mattered for the immune response.
- primary_references
- [creatine-p35235777] Creatine transport and creatine kinase activity is required for CD8+ T cell immunity. (2022). https://pubmed.ncbi.nlm.nih.gov/35235777/ DOI: 10.1016/j.celrep.2022.110446
- tissue_or_cell_type
- Naive and activated CD8 T cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 607–618
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter or kinase loss, T-cell homeostasis and infection experiments · source_derived_draft · unverified_draft
### creatine-tcell-expansion-loss Loss of either Ckb or Slc6a8 compromised CD8 T-cell expansion in response to infection. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Both the transporter and the phosphate-transfer enzyme mattered for the immune response. organism: Mice tissue_or_cell_type: Naive and activated CD8 T cells experimental_model: Transporter or kinase loss, T-cell homeostasis and infection experiments limitations: The study distinguishes TCR–mTORC1 signaling from whole-cell adenylate energy charge; it does not demonstrate clinical immune benefits of supplements. exposure: Slc6a8 or Ckb deletion evidence_span: {"source_cache": "artifacts/creatine-research/35235777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958", "start_char": 0, "end_char": 1025, "text_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958"} [creatine-p35235777] Creatine transport and creatine kinase activity is required for CD8+ T cell immunity. (2022). https://pubmed.ncbi.nlm.nih.gov/35235777/ DOI: 10.1016/j.celrep.2022.110446
Complete structured claim and evidenceCkb or Slc6a8 loss weakened TCR-mediated mTORC1 activation required for CD8 T-cell expansion.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/creatine-research/35235777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958", "start_char": 0, "end_char": 1025, "text_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958"}
- experimental_model
- Transporter or kinase loss, T-cell homeostasis and infection experiments
- exposure
- Slc6a8 or Ckb deletion
- limitations
- The study distinguishes TCR–mTORC1 signaling from whole-cell adenylate energy charge; it does not demonstrate clinical immune benefits of supplements.
- nutrient_topic
- Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
- organism
- Mice
- plain_language
- The pathway also affected the signal telling T cells to expand.
- primary_references
- [creatine-p35235777] Creatine transport and creatine kinase activity is required for CD8+ T cell immunity. (2022). https://pubmed.ncbi.nlm.nih.gov/35235777/ DOI: 10.1016/j.celrep.2022.110446
- tissue_or_cell_type
- Naive and activated CD8 T cells
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 620–631
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter or kinase loss, T-cell homeostasis and infection experiments · source_derived_draft · unverified_draft
### creatine-tcell-mtor-loss Ckb or Slc6a8 loss weakened TCR-mediated mTORC1 activation required for CD8 T-cell expansion. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The pathway also affected the signal telling T cells to expand. organism: Mice tissue_or_cell_type: Naive and activated CD8 T cells experimental_model: Transporter or kinase loss, T-cell homeostasis and infection experiments limitations: The study distinguishes TCR–mTORC1 signaling from whole-cell adenylate energy charge; it does not demonstrate clinical immune benefits of supplements. exposure: Slc6a8 or Ckb deletion evidence_span: {"source_cache": "artifacts/creatine-research/35235777.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958", "start_char": 0, "end_char": 1025, "text_sha256": "a81515a03473f41d52c2e13de56ac9b13ea5cd813e288d166159d517f9855958"} [creatine-p35235777] Creatine transport and creatine kinase activity is required for CD8+ T cell immunity. (2022). https://pubmed.ncbi.nlm.nih.gov/35235777/ DOI: 10.1016/j.celrep.2022.110446
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.