Human creatine transporter CRT / SLC6A8

What it acts on

1. Human creatine-transporter expression conferred sodium-dependent creatine uptake with Km 14.9 ± 3.0 micromolar in five experiments.

   Human creatine transporter CRT / SLC6A8 → Creatine source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/sodium-research/7945388.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4f936121279583ab698555d2a318900a9dc5a42ecbf294619ee3abcc95c9a2f0", "start_char": 0, "end_char": 910, "text_sha256": "4f936121279583ab698555d2a318900a9dc5a42ecbf294619ee3abcc95c9a2f0"}

   experimental_model

   Cloning and functional expression

   exposure

   Radiolabeled creatine uptake

   limitations

   This primary abstract establishes sodium dependence; no chloride stoichiometry or clinical benefit is inferred.

   nutrient_topic

   Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium

   organism

   Human SLC6A8 in COS-7 cells

   plain_language

   Creatine entry has its own sodium-coupled transporter.

   primary_references

   [sodium-p7945388] The cloning and expression of a human creatine transporter. (1994). https://pubmed.ncbi.nlm.nih.gov/7945388/ DOI: 10.1006/bbrc.1994.2475

   tissue_or_cell_type

   Cell plasma membrane

   transport_effect

   raises Expression conferred sodium-dependent creatine uptake.

   transport_pool

   the expressing cell Expression conferred sodium-dependent creatine uptake.

   Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 629–640

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cloning and functional expression · source_derived_draft · unverified_draft

   ### sodium-creatine-transport Human creatine-transporter expression conferred sodium-dependent creatine uptake with Km 14.9 ± 3.0 micromolar in five experiments. Condition category: normal nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Creatine entry has its own sodium-coupled transporter. organism: Human SLC6A8 in COS-7 cells tissue_or_cell_type: Cell plasma membrane experimental_model: Cloning and functional expression limitations: This primary abstract establishes sodium dependence; no chloride stoichiometry or clinical benefit is inferred. exposure: Radiolabeled creatine uptake evidence_span: {"source_cache": "artifacts/sodium-research/7945388.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4f936121279583ab698555d2a318900a9dc5a42ecbf294619ee3abcc95c9a2f0", "start_char": 0, "end_char": 910, "text_sha256": "4f936121279583ab698555d2a318900a9dc5a42ecbf294619ee3abcc95c9a2f0"} [sodium-p7945388] The cloning and expression of a human creatine transporter. (1994). https://pubmed.ncbi.nlm.nih.gov/7945388/ DOI: 10.1006/bbrc.1994.2475

   Complete structured claim and evidence

2. The high-affinity component of creatine accumulation and AGAT regulation depended on SLC6A8, whereas a nonsaturable component remained without the transporter.

   Human creatine transporter CRT / SLC6A8 → Intracellular creatine content source_derived_draftungraded
   Experimental context and source evidence

   evidence_span

   {"source_cache": "artifacts/creatine-research/38104212.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936", "start_char": 0, "end_char": 1889, "text_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936"}

   experimental_model

   CRISPR AGAT reporter, transporter knockout and rescue

   exposure

   Manipulated extracellular and intracellular creatine with intact or deleted SLC6A8

   limitations

   Cell-line reporter regulation; the intracellular sensor was inferred rather than molecularly identified.

   nutrient_topic

   Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine

   organism

   Human HAP1 cells

   plain_language

   The usual transporter shaped feedback, but the engineered cells also showed a separate low-affinity route.

   primary_references

   [creatine-p38104212] Evidence of an intracellular creatine-sensing mechanism that modulates creatine biosynthesis via AGAT expression in human HAP1 cells. (2023). https://pubmed.ncbi.nlm.nih.gov/38104212/ DOI: 10.1038/s41598-023-49860-1

   tissue_or_cell_type

   Cultured cells

   Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 321–332

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CRISPR AGAT reporter, transporter knockout and rescue · source_derived_draft · unverified_draft

   ### creatine-feedback-transporter-component The high-affinity component of creatine accumulation and AGAT regulation depended on SLC6A8, whereas a nonsaturable component remained without the transporter. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The usual transporter shaped feedback, but the engineered cells also showed a separate low-affinity route. organism: Human HAP1 cells tissue_or_cell_type: Cultured cells experimental_model: CRISPR AGAT reporter, transporter knockout and rescue limitations: Cell-line reporter regulation; the intracellular sensor was inferred rather than molecularly identified. exposure: Manipulated extracellular and intracellular creatine with intact or deleted SLC6A8 evidence_span: {"source_cache": "artifacts/creatine-research/38104212.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936", "start_char": 0, "end_char": 1889, "text_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936"} [creatine-p38104212] Evidence of an intracellular creatine-sensing mechanism that modulates creatine biosynthesis via AGAT expression in human HAP1 cells. (2023). https://pubmed.ncbi.nlm.nih.gov/38104212/ DOI: 10.1038/s41598-023-49860-1

   Complete structured claim and evidence

3. CRT loss impaired epithelial barrier formation and wound healing; transporter-deficient organoids also had reduced barrier function.

   Human creatine transporter CRT / SLC6A8 → Intestinal epithelial barrier integrity source_derived_draftungraded
   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 evidence

4. CRT loss increased epithelial glycolytic stress and was accompanied by actin mislocalization and leaky junctions.

   Human creatine transporter CRT / SLC6A8 → Intestinal epithelial glycolytic stress source_derived_draftungraded
   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

   The transporter defect changed both energy handling and the cell structures that seal the barrier.

   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 659–670

   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-stress CRT loss increased epithelial glycolytic stress and was accompanied by actin mislocalization and leaky junctions. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The transporter defect changed both energy handling and the cell structures that seal the barrier. 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 evidence

5. Intestinal CRT transcript expression was lower in the Crohn disease and ulcerative colitis biopsy groups than in controls.

   Human creatine transporter CRT / SLC6A8 → Intestinal creatine transporter expression source_derived_draftungraded
   Experimental context and source evidence

   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

   Humans

   plain_language

   The human tissue comparison found an association; it did not show that reduced creatine intake caused bowel disease.

   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 biopsies

   Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 672–683

   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-ibd-crt-expression Intestinal CRT transcript expression was lower in the Crohn disease and ulcerative colitis biopsy groups than in controls. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The human tissue comparison found an association; it did not show that reduced creatine intake caused bowel disease. organism: Humans tissue_or_cell_type: Intestinal biopsies 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 evidence

6. The SLC6A8-deficient male had absent brain creatine on spectroscopy and defective fibroblast creatine uptake despite high plasma and urinary creatine and normal guanidinoacetate.

   Human creatine transporter CRT / SLC6A8 → Brain total creatine concentration source_derived_draftungraded
   Experimental context and source evidence

   availability_state

   machinery_impairment Imported condition classification; unverified.

   evidence_span

   {"source_cache": "artifacts/creatine-research/11326334.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95d65dd9212e917935c2c5d5c76a36a1bef2803c23be600da6b2e1c54bcd5cc9", "start_char": 0, "end_char": 739, "text_sha256": "95d65dd9212e917935c2c5d5c76a36a1bef2803c23be600da6b2e1c54bcd5cc9"}

   experimental_model

   Human family genetics and fibroblast transport assay

   exposure

   SLC6A8 loss-of-function variant

   limitations

   Single family; circulating creatine cannot substitute for cellular transport. No treatment failure claim is inferred from this abstract.

   nutrient_topic

   Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine

   organism

   Human male patient and relatives

   plain_language

   A high blood or urine value did not mean creatine reached the brain.

   primary_references

   [creatine-p11326334] X-linked creatine-transporter gene (SLC6A8) defect: a new creatine-deficiency syndrome. (2001). https://pubmed.ncbi.nlm.nih.gov/11326334/ DOI: 10.1086/320595

   tissue_or_cell_type

   Brain spectroscopy, plasma, urine and fibroblasts

   trigger_kind

   machinery_impairment Imported condition classification; unverified.

   Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 906–917

   AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human family genetics and fibroblast transport assay · source_derived_draft · unverified_draft

   ### creatine-transporter-brain-loss The SLC6A8-deficient male had absent brain creatine on spectroscopy and defective fibroblast creatine uptake despite high plasma and urinary creatine and normal guanidinoacetate. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A high blood or urine value did not mean creatine reached the brain. organism: Human male patient and relatives tissue_or_cell_type: Brain spectroscopy, plasma, urine and fibroblasts experimental_model: Human family genetics and fibroblast transport assay limitations: Single family; circulating creatine cannot substitute for cellular transport. No treatment failure claim is inferred from this abstract. exposure: SLC6A8 loss-of-function variant evidence_span: {"source_cache": "artifacts/creatine-research/11326334.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "95d65dd9212e917935c2c5d5c76a36a1bef2803c23be600da6b2e1c54bcd5cc9", "start_char": 0, "end_char": 739, "text_sha256": "95d65dd9212e917935c2c5d5c76a36a1bef2803c23be600da6b2e1c54bcd5cc9"} [creatine-p11326334] X-linked creatine-transporter gene (SLC6A8) defect: a new creatine-deficiency syndrome. (2001). https://pubmed.ncbi.nlm.nih.gov/11326334/ DOI: 10.1086/320595

   Complete structured claim and evidence