{"id":"d19bd22f-6403-5035-8fbb-5b58e401a57b","stable_key":"aaa7baba-8689-56ab-ba1e-b71542bcb8e9:iodine-trans-a7-no-efflux2018","predicate":"does_not_increase","statement":"Cangul et al. found no enhancement of radioiodide efflux from HEK293 cells coexpressing human NIS and SLC26A7 compared with control cells, whereas pendrin enhanced efflux.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"neutral","is_public":true,"mechanism_event_id":"fea1074d-8731-58b1-a2be-40ca5680f1d1","mechanism_event_label":"An earlier cell assay did not detect an iodide export effect from SLC26A7.","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":"fea1074d-8731-58b1-a2be-40ca5680f1d1","stable_key":"aaa7baba-8689-56ab-ba1e-b71542bcb8e9:iodine-trans-a7-no-efflux2018-event","event_type":"biochemical_relationship","label":"An earlier cell assay did not detect an iodide export effect from SLC26A7.","description":"Cangul et al. found no enhancement of radioiodide efflux from HEK293 cells coexpressing human NIS and SLC26A7 compared with control cells, whereas pendrin enhanced efflux.","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":"loading_transporter","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"57fef31d-e7e6-5b6f-aee1-77fb94592ce7","slug":"slc26a4","display_name":"Human pendrin / SLC26A4","entity_type_key":"protein"},"role":"positive_control","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"83b11ca6-52c7-5a1b-8c39-d9cdf89244e3","slug":"iodide","display_name":"Iodide ion","entity_type_key":"ion"},"role":"assayed_substrate","stoichiometry":null,"state_label":"","sequence_order":2,"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":3,"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":4,"notes":""}]},"contexts":[{"dimension":"cross_nutrient","value_text":"false","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Six human families, human SLC26A7/NIS-transfected HEK293 cells, Slc26a7-null mice","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"NIS plus SLC26A7, pendrin or control expression; time-dependent radioiodide efflux; five experiments, Fig. 2E.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"A negative result in this assay is not proof that SLC26A7 never conducts iodide; later positive transport and structural evidence is retained.","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":"Homo sapiens protein and HEK293 cells","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"An earlier cell assay did not detect an iodide export effect from SLC26A7.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[iodine-trans-slc26a7-2018] Homozygous loss-of-function mutations in SLC26A7 cause goitrous congenital hypothyroidism. (2018). https://pubmed.ncbi.nlm.nih.gov/30333321/ DOI: 10.1172/jci.insight.99631","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Cultured-cell plasma membrane","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"d2c9ffd6-a43f-5fc3-8799-28192b6ce2d0","evidence_kind":"source_excerpt","locator":"Lines 375-386","start_line":375,"end_line":386,"excerpt":"### iodine-trans-a7-no-efflux2018\nCangul et al. found no enhancement of radioiodide efflux from HEK293 cells coexpressing human NIS and SLC26A7 compared with control cells, whereas pendrin enhanced efflux.\nCondition category: normal\nnutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: An earlier cell assay did not detect an iodide export effect from SLC26A7.\norganism: Homo sapiens protein and HEK293 cells\ntissue_or_cell_type: Cultured-cell plasma membrane\nexperimental_model: Six human families, human SLC26A7/NIS-transfected HEK293 cells, Slc26a7-null mice\nlimitations: A negative result in this assay is not proof that SLC26A7 never conducts iodide; later positive transport and structural evidence is retained.\nexposure: NIS plus SLC26A7, pendrin or control expression; time-dependent radioiodide efflux; five experiments, Fig. 2E.\ncross_nutrient: false\n[iodine-trans-slc26a7-2018] Homozygous loss-of-function mutations in SLC26A7 cause goitrous congenital hypothyroidism. (2018). https://pubmed.ncbi.nlm.nih.gov/30333321/ DOI: 10.1172/jci.insight.99631","model_system":"Six human families, human SLC26A7/NIS-transfected HEK293 cells, Slc26a7-null mice","directness":"author_interpretation","verification_status":"source_derived_draft","notes":"Exact curation-document quotation, not publisher quotation. Study references: [iodine-trans-slc26a7-2018] Homozygous loss-of-function mutations in SLC26A7 cause goitrous congenital hypothyroidism. (2018). https://pubmed.ncbi.nlm.nih.gov/30333321/ DOI: 10.1172/jci.insight.99631","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}