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(2023). https://pubmed.ncbi.nlm.nih.gov/38104212/ DOI: 10.1038/s41598-023-49860-1","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Cultured cells","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"b48bcbdb-9d4d-5f2f-bc5a-46b4855f3a79","evidence_kind":"source_excerpt","locator":"Lines 321-332","start_line":321,"end_line":332,"excerpt":"### creatine-feedback-transporter-component\nThe high-affinity component of creatine accumulation and AGAT regulation depended on SLC6A8, whereas a nonsaturable component remained without the transporter.\nCondition category: normal\nnutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: The usual transporter shaped feedback, but the engineered cells also showed a separate low-affinity route.\norganism: Human HAP1 cells\ntissue_or_cell_type: Cultured cells\nexperimental_model: CRISPR AGAT reporter, transporter knockout and rescue\nlimitations: Cell-line reporter regulation; the intracellular sensor was inferred rather than molecularly identified.\nexposure: Manipulated extracellular and intracellular creatine with intact or deleted SLC6A8\nevidence_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\"}\n[creatine-p38104212] Evidence of an intracellular creatine-sensing mechanism that modulates creatine biosynthesis via AGAT expression in human HAP1 cells. 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