{"id":"9c461829-cb41-5e38-8e85-2980a7fad76c","stable_key":"d96b230c-481b-535b-930c-04eb87ec7f02:s-allylcysteine-colon-ahr","predicate":"reduces_tested_signaling_of","statement":"SAC treatment reduced AhR-pathway signaling during PhIP challenge.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"negative","is_public":true,"mechanism_event_id":"0173974c-66c8-5d2f-b613-71f4ab54a63e","mechanism_event_label":"Carcinogen-response signaling changed alongside redox defenses.","subject":{"id":"8c2c295d-68b3-5e62-b1a7-00fcf915e3cc","slug":"s-allylcysteine","display_name":"S-allyl-L-cysteine / SAC","entity_type_key":"small_molecule"},"object":{"id":"757ea2d0-1c8e-5453-a721-4a3a3443a383","slug":"ahr","display_name":"Human aryl hydrocarbon receptor / AHR","entity_type_key":"protein"},"evidence_count":1,"mechanism_event":{"id":"0173974c-66c8-5d2f-b613-71f4ab54a63e","stable_key":"d96b230c-481b-535b-930c-04eb87ec7f02:s-allylcysteine-colon-ahr-event","event_type":"observed_relationship","label":"Carcinogen-response signaling changed alongside redox defenses.","description":"SAC treatment reduced AhR-pathway signaling during PhIP challenge.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"8c2c295d-68b3-5e62-b1a7-00fcf915e3cc","slug":"s-allylcysteine","display_name":"S-allyl-L-cysteine / SAC","entity_type_key":"small_molecule"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"757ea2d0-1c8e-5453-a721-4a3a3443a383","slug":"ahr","display_name":"Human aryl hydrocarbon receptor / AHR","entity_type_key":"protein"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""}]},"contexts":[{"dimension":"acting_entity","value_text":"s-allylcysteine","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"dose","value_text":"Not specified in accessed abstract","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"duration","value_text":"Not specified in accessed abstract","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"evidence_access","value_text":"Primary abstract","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_comparison","value_text":"SAC with PhIP challenge and corresponding cell controls","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Normal human colonic mucosal epithelial cells exposed to PhIP","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"interpretation_status","value_text":"Source-derived research curation; not independent primary verification","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Does not quantify a clinical drug interaction or prove reduced carcinogen activation in people.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"S-allylcysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit.","comparator":null,"unit":null,"notes":"","entity":{"slug":"s-allylcysteine","display_name":"S-allyl-L-cysteine / SAC","entity_type_key":"small_molecule"}},{"dimension":"organism","value_text":"Homo sapiens","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"Carcinogen-response signaling changed alongside redox defenses.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[35753083] S-Allylcysteine Potently Protects against PhIP-Induced DNA Damage via Nrf2/AhR Signaling Pathway Modulation in Normal Human Colonic Mucosal Epithelial Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35753083/ · DOI 10.1002/mnfr.202101141","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"route","value_text":"Cell culture","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Normal human colonic mucosal epithelial cells exposed to PhIP","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"5a4c49ba-8b45-5565-804c-f9b4695073d0","evidence_kind":"source_excerpt","locator":"Lines 167-174","start_line":167,"end_line":174,"excerpt":"## s-allylcysteine-colon-ahr\nCarcinogen-response signaling changed alongside redox defenses.\nSAC treatment reduced AhR-pathway signaling during PhIP challenge.\nModel: Normal human colonic mucosal epithelial cells exposed to PhIP\nLimitations: Does not quantify a clinical drug interaction or prove reduced carcinogen activation in people.\nEvidence access: Primary abstract\n[35753083] S-Allylcysteine Potently Protects against PhIP-Induced DNA Damage via Nrf2/AhR Signaling Pathway Modulation in Normal Human Colonic Mucosal Epithelial Cells. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35753083/ · DOI 10.1002/mnfr.202101141\nStructured context: {\"organism\": \"Homo sapiens\", \"tissue_or_cell_type\": \"Normal human colonic mucosal epithelial cells exposed to PhIP\", \"dose\": \"Not specified in accessed abstract\", \"duration\": \"Not specified in accessed abstract\", \"route\": \"Cell culture\", \"experimental_comparison\": \"SAC with PhIP challenge and corresponding cell controls\", \"acting_entity\": \"s-allylcysteine\", \"interpretation_status\": \"Source-derived research curation; not independent primary verification\"}","model_system":"Normal human colonic mucosal epithelial cells exposed to PhIP","directness":"reported_statement","verification_status":"source_derived_draft","notes":"Original curation paraphrase; evidence access and experimental limitations specified.","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"3b0d58f9-8a69-579d-9920-518399a9a8bb","stable_key":"import-d96b230c-481b-535b-930c-04eb87ec7f02","title":"S-allylcysteine: sulfur signaling, redox responses and cross-nutrient mechanisms (2026-09-20)","document_type":"imported_text","citation_label":"AI-assisted research curation; primary references, access levels and experimental limitations individually identified. 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