{"id":"f196a827-30d7-54f5-a8c4-8b5faf1b0a6f","stable_key":"aaa7baba-8689-56ab-ba1e-b71542bcb8e9:iodine-trans-a7-efflux2019","predicate":"promotes","statement":"MDCK monolayers coexpressing human NIS and SLC26A7 transferred more basal-chamber radioiodide into the apical chamber after 45 minutes than monolayers expressing NIS alone.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"positive","is_public":true,"mechanism_event_id":"923d7eb8-dca8-5bfd-b300-0a010b1fc07f","mechanism_event_label":"SLC26A7 increased iodide movement across a polarized cell sheet in this experiment.","subject":{"id":"6ae2ac42-e051-59b1-aabb-f8263f987ea4","slug":"slc26a7","display_name":"Human SLC26A7 anion transporter","entity_type_key":"protein"},"object":{"id":"99611171-98f5-5310-af88-a988e8f0e6a6","slug":"cellular-iodide-efflux","display_name":"Cellular iodide efflux","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"923d7eb8-dca8-5bfd-b300-0a010b1fc07f","stable_key":"aaa7baba-8689-56ab-ba1e-b71542bcb8e9:iodine-trans-a7-efflux2019-event","event_type":"biochemical_relationship","label":"SLC26A7 increased iodide movement across a polarized cell sheet in this experiment.","description":"MDCK monolayers coexpressing human NIS and SLC26A7 transferred more basal-chamber radioiodide into the apical chamber after 45 minutes than monolayers expressing NIS alone.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"0d051c22-c0d2-5c22-91ad-4ee6894dc7a0","slug":"slc5a5","display_name":"Human sodium/iodide symporter / SLC5A5","entity_type_key":"protein"},"role":"basal_loading_transporter","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"83b11ca6-52c7-5a1b-8c39-d9cdf89244e3","slug":"iodide","display_name":"Iodide ion","entity_type_key":"ion"},"role":"transported_substrate","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"6ae2ac42-e051-59b1-aabb-f8263f987ea4","slug":"slc26a7","display_name":"Human SLC26A7 anion transporter","entity_type_key":"protein"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""},{"entity":{"id":"99611171-98f5-5310-af88-a988e8f0e6a6","slug":"cellular-iodide-efflux","display_name":"Cellular iodide efflux","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":3,"notes":""}]},"contexts":[{"dimension":"cross_nutrient","value_text":"false","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Human thyroid tissue; recombinant human SLC26A7 in Nthy, MDCK, COS-7 and HEK293T cells; two affected siblings","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"Induced transporter expression 24 hours before assay; basal radioactive NaI and 45-minute transport readout; Fig. 3c.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"A 2018 HEK293 efflux assay was negative. This experiment establishes capability under its conditions, not universal apical placement in human thyroid.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Iodine research collection; topical membership is not evidence of a direct dietary effect.","comparator":null,"unit":null,"notes":"","entity":{"slug":"iodine","display_name":"Iodine","entity_type_key":"nutrient_element"}},{"dimension":"organism","value_text":"Human proteins in canine MDCK cells","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"SLC26A7 increased iodide movement across a polarized cell sheet in this experiment.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[iodine-trans-slc26a7-2019] Congenital goitrous hypothyroidism is caused by dysfunction of the iodide transporter SLC26A7. (2019). https://pubmed.ncbi.nlm.nih.gov/31372509/ DOI: 10.1038/s42003-019-0503-6","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Polarized epithelial bicameral culture","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"8d52c8b7-41e5-5a44-8ac3-784461c6dda1","evidence_kind":"source_excerpt","locator":"Lines 336-347","start_line":336,"end_line":347,"excerpt":"### iodine-trans-a7-efflux2019\nMDCK monolayers coexpressing human NIS and SLC26A7 transferred more basal-chamber radioiodide into the apical chamber after 45 minutes than monolayers expressing NIS alone.\nCondition category: normal\nnutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: SLC26A7 increased iodide movement across a polarized cell sheet in this experiment.\norganism: Human proteins in canine MDCK cells\ntissue_or_cell_type: Polarized epithelial bicameral culture\nexperimental_model: Human thyroid tissue; recombinant human SLC26A7 in Nthy, MDCK, COS-7 and HEK293T cells; two affected siblings\nlimitations: A 2018 HEK293 efflux assay was negative. This experiment establishes capability under its conditions, not universal apical placement in human thyroid.\nexposure: Induced transporter expression 24 hours before assay; basal radioactive NaI and 45-minute transport readout; Fig. 3c.\ncross_nutrient: false\n[iodine-trans-slc26a7-2019] Congenital goitrous hypothyroidism is caused by dysfunction of the iodide transporter SLC26A7. (2019). https://pubmed.ncbi.nlm.nih.gov/31372509/ DOI: 10.1038/s42003-019-0503-6","model_system":"Human thyroid tissue; recombinant human SLC26A7 in Nthy, MDCK, COS-7 and HEK293T cells; two affected siblings","directness":"author_interpretation","verification_status":"source_derived_draft","notes":"Exact curation-document quotation, not publisher quotation. Study references: [iodine-trans-slc26a7-2019] Congenital goitrous hypothyroidism is caused by dysfunction of the iodide transporter SLC26A7. (2019). https://pubmed.ncbi.nlm.nih.gov/31372509/ DOI: 10.1038/s42003-019-0503-6","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"76da623d-a34a-5a5c-a942-d7571a85c486","stable_key":"import-aaa7baba-8689-56ab-ba1e-b71542bcb8e9","title":"Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17)","document_type":"imported_text","citation_label":"AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text.","file_path":"","sha256":"a4885eb6f58bad4a4514c958b63834619e57b10aa7f694aa97d0f65c7d36548f","revision_id":"ea8001a1-b576-5eda-a193-883c7ad59b73","review_status":"unverified_draft","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}