{"id":"09d82b35-1669-5691-9d6b-5dc141aa495f","stable_key":"507ed066-fd6d-5722-9223-97b66302e7e3:glycine-glyt2-loss","predicate":"supports","statement":"Deleting mouse Slc6a5 reduced glycinergic miniature inhibitory-current amplitudes in hypoglossal motoneurons and dissociated spinal neurons.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"context_dependent","is_public":true,"mechanism_event_id":"32abcd86-8b22-59d2-b6c2-d06ac3df26a7","mechanism_event_label":"Loss of replenishment machinery weakens inhibitory transmitter output.","subject":{"id":"f692570f-34a4-58ec-8ef6-e953ff616093","slug":"mouse-slc6a5","display_name":"Mouse glycine transporter 2 / Slc6a5","entity_type_key":"protein"},"object":{"id":"b04cf89d-1a33-5591-91e5-252de44ae0ad","slug":"mouse-glycinergic-mipsc","display_name":"Mouse glycinergic miniature inhibitory postsynaptic currents","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"32abcd86-8b22-59d2-b6c2-d06ac3df26a7","stable_key":"507ed066-fd6d-5722-9223-97b66302e7e3:glycine-glyt2-loss-event","event_type":"observed_relationship","label":"Loss of replenishment machinery weakens inhibitory transmitter output.","description":"Deleting mouse Slc6a5 reduced glycinergic miniature inhibitory-current amplitudes in hypoglossal motoneurons and dissociated spinal neurons.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"f692570f-34a4-58ec-8ef6-e953ff616093","slug":"mouse-slc6a5","display_name":"Mouse glycine transporter 2 / Slc6a5","entity_type_key":"protein"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"b04cf89d-1a33-5591-91e5-252de44ae0ad","slug":"mouse-glycinergic-mipsc","display_name":"Mouse glycinergic miniature inhibitory postsynaptic currents","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"2b507258-430c-51fe-9fd2-e510c2c197a9","slug":"glycine","display_name":"Glycine","entity_type_key":"small_molecule"},"role":"context_participant","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""}]},"contexts":[{"dimension":"availability_state","value_text":"machinery_impairment","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null},{"dimension":"evidence_access","value_text":"Primary abstract","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Mouse knockout; neuronal electrophysiology and postnatal neuromotor phenotype.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Transporter deletion is not dietary glycine deficiency.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Glycine collection; species, compartment, exposure, co-substrates and manipulation remain explicit.","comparator":null,"unit":null,"notes":"","entity":{"slug":"glycine","display_name":"Glycine","entity_type_key":"small_molecule"}},{"dimension":"plain_language","value_text":"Loss of replenishment machinery weakens inhibitory transmitter output.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"Deletion of the mouse glycine transporter 2 results in a hyperekplexia phenotype and postnatal lethality. · 2003 · https://pubmed.ncbi.nlm.nih.gov/14622583/ · DOI 10.1016/s0896-6273(03)00673-1","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"trigger_kind","value_text":"machinery_impairment","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null}],"evidence":[{"id":"eef47fd0-058b-572e-aaff-f22d5e94bf57","evidence_kind":"source_excerpt","locator":"Lines 50-56","start_line":50,"end_line":56,"excerpt":"## glycine-glyt2-loss\nLoss of replenishment machinery weakens inhibitory transmitter output.\nDeleting mouse Slc6a5 reduced glycinergic miniature inhibitory-current amplitudes in hypoglossal motoneurons and dissociated spinal neurons.\nModel: Mouse knockout; neuronal electrophysiology and postnatal neuromotor phenotype.\nLimitations: Transporter deletion is not dietary glycine deficiency.\nEvidence access: Primary abstract\nDeletion of the mouse glycine transporter 2 results in a hyperekplexia phenotype and postnatal lethality. · 2003 · https://pubmed.ncbi.nlm.nih.gov/14622583/ · DOI 10.1016/s0896-6273(03)00673-1","model_system":"Mouse knockout; neuronal electrophysiology and postnatal neuromotor phenotype.","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":"7b2859d8-e2bf-51e7-8e32-0715c10cbc49","stable_key":"import-507ed066-fd6d-5722-9223-97b66302e7e3","title":"Glycine: supply, one-carbon allocation, receptors 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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