{"id":"3f3c0b23-6fa8-5cf4-8222-214590fe811e","stable_key":"e37461ea-ea5d-5e2c-8091-138305f6dd70:l-aspartate-eaat1-hypoxia","predicate":"supports_growth_under_hypoxia","statement":"Increasing SLC1A3-mediated uptake supplied aspartate for nucleotide synthesis and improved proliferation under low oxygen and growth in tumor xenograft models.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"7e6c2acb-8ded-5cfd-9c82-76dd8b0b3d52","mechanism_event_label":"Uptake partly bypassed a synthesis bottleneck in the tested tumors.","subject":{"id":"23bdf240-9ac3-57fc-8270-af878c463361","slug":"slc1a3","display_name":"Human excitatory amino acid transporter 1 / SLC1A3","entity_type_key":"protein"},"object":{"id":"f64e0df7-2122-5130-ac1d-fcf24de35767","slug":"human-cancer-hypoxic-proliferation","display_name":"Hypoxic proliferation of human cancer cells","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"7e6c2acb-8ded-5cfd-9c82-76dd8b0b3d52","stable_key":"e37461ea-ea5d-5e2c-8091-138305f6dd70:l-aspartate-eaat1-hypoxia-event","event_type":"observed_relationship","label":"Uptake partly bypassed a synthesis bottleneck in the tested tumors.","description":"Increasing SLC1A3-mediated uptake supplied aspartate for nucleotide synthesis and improved proliferation under low oxygen and growth in tumor xenograft models.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"23bdf240-9ac3-57fc-8270-af878c463361","slug":"slc1a3","display_name":"Human excitatory amino acid transporter 1 / SLC1A3","entity_type_key":"protein"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"f64e0df7-2122-5130-ac1d-fcf24de35767","slug":"human-cancer-hypoxic-proliferation","display_name":"Hypoxic proliferation of human cancer cells","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"0a0923d3-72b7-5d6a-bf3a-5a7a3071a09b","slug":"l-aspartate","display_name":"L-Aspartate","entity_type_key":"small_molecule"},"role":"context_participant","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""},{"entity":{"id":"7da684a4-2641-5bc6-93ae-8c6aa384e487","slug":"glutamate","display_name":"L-Glutamate","entity_type_key":"small_molecule"},"role":"context_participant","stoichiometry":null,"state_label":"","sequence_order":3,"notes":""}]},"contexts":[{"dimension":"evidence_access","value_text":"Primary full text","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Human cancer cultures and xenografts in immunodeficient mice.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Not every tumor expresses this transporter, and this is not evidence that ordinary intake initiates cancer. Correction record: The 2018 author correction added a missing competing-interests statement declaring no competing interests; no mechanism or data change was stated. PMID 30089842; DOI 10.1038/s41556-018-0184-2. https://pubmed.ncbi.nlm.nih.gov/30089842/","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit.","comparator":null,"unit":null,"notes":"","entity":{"slug":"l-aspartate","display_name":"L-Aspartate","entity_type_key":"small_molecule"}},{"dimension":"plain_language","value_text":"Uptake partly bypassed a synthesis bottleneck in the tested tumors.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"Aspartate is a limiting metabolite for cancer cell proliferation under hypoxia and in tumours. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29941933/ · DOI 10.1038/s41556-018-0118-z","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"2a85d43a-7850-50bf-9025-ae93370b7bb3","evidence_kind":"source_excerpt","locator":"Lines 82-88","start_line":82,"end_line":88,"excerpt":"## l-aspartate-eaat1-hypoxia\nUptake partly bypassed a synthesis bottleneck in the tested tumors.\nIncreasing SLC1A3-mediated uptake supplied aspartate for nucleotide synthesis and improved proliferation under low oxygen and growth in tumor xenograft models.\nModel: Human cancer cultures and xenografts in immunodeficient mice.\nLimitations: Not every tumor expresses this transporter, and this is not evidence that ordinary intake initiates cancer. Correction record: The 2018 author correction added a missing competing-interests statement declaring no competing interests; no mechanism or data change was stated. PMID 30089842; DOI 10.1038/s41556-018-0184-2. https://pubmed.ncbi.nlm.nih.gov/30089842/\nEvidence access: Primary full text\nAspartate is a limiting metabolite for cancer cell proliferation under hypoxia and in tumours. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29941933/ · DOI 10.1038/s41556-018-0118-z","model_system":"Human cancer cultures and xenografts in immunodeficient mice.","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":"67970dcb-34e0-5b0a-8c86-d8c3cc183444","stable_key":"import-e37461ea-ea5d-5e2c-8091-138305f6dd70","title":"L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19)","document_type":"imported_text","citation_label":"AI-assisted research curation; primary references, access levels and experimental limitations individually identified. 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