PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
17693006-2	2007	Studies have shown that the brain N-acetyl aspartate (NAA) levels are greatly decreased in aralar-deficient mice, suggesting that aralar plays an important role in the synthesis of NAA in neuronal cells.	N-acetylaspartate	34-52	solute carrier family 25 member 12	Homo sapiens	91-97	
17693006-2	2007	Studies have shown that the brain N-acetyl aspartate (NAA) levels are greatly decreased in aralar-deficient mice, suggesting that aralar plays an important role in the synthesis of NAA in neuronal cells.	N-acetylaspartate	54-57	solute carrier family 25 member 12	Homo sapiens	91-97	
17693006-2	2007	Studies have shown that the brain N-acetyl aspartate (NAA) levels are greatly decreased in aralar-deficient mice, suggesting that aralar plays an important role in the synthesis of NAA in neuronal cells.	N-acetylaspartate	181-184	solute carrier family 25 member 12	Homo sapiens	91-97	
17693006-3	2007	Since magnetic resonance spectroscopy studies have revealed consistently reduced NAA levels in various brain regions of schizophrenic patients and their unaffected relatives, genes that affect aralar levels or NAA metabolism in the brain may be implicated in the pathogenesis of schizophrenia.	N-acetylaspartate	81-84	solute carrier family 25 member 12	Homo sapiens	193-199	
17693006-9	2007	Further studies with SLC25A12 variants relating to brain NAA levels in patients with schizophrenia are suggested.	N-acetylaspartate	57-60	solute carrier family 25 member 12	Homo sapiens	21-29	
24515575-10	2014	One prior reported SLC25A12 mutation caused complete loss of AGC1 activity in a child with epilepsy, hypotonia, hypomyelination, and reduced brain NAA.	N-acetylaspartate	147-150	solute carrier family 25 member 12	Homo sapiens	19-27	
35008954-2	2022	The deficiency in AGC1/Aralar leads to the human rare disease named "early infantile epileptic encephalopathy 39" (EIEE 39, OMIM # 612949) characterized by epilepsy, hypotonia, arrested psychomotor neurodevelopment, hypo myelination and a drastic drop in brain aspartate (Asp) and N-acetylaspartate (NAA).	N-acetylaspartate	281-298	solute carrier family 25 member 12	Homo sapiens	18-22	
35008954-2	2022	The deficiency in AGC1/Aralar leads to the human rare disease named "early infantile epileptic encephalopathy 39" (EIEE 39, OMIM # 612949) characterized by epilepsy, hypotonia, arrested psychomotor neurodevelopment, hypo myelination and a drastic drop in brain aspartate (Asp) and N-acetylaspartate (NAA).	N-acetylaspartate	281-298	solute carrier family 25 member 12	Homo sapiens	23-29	
35008954-2	2022	The deficiency in AGC1/Aralar leads to the human rare disease named "early infantile epileptic encephalopathy 39" (EIEE 39, OMIM # 612949) characterized by epilepsy, hypotonia, arrested psychomotor neurodevelopment, hypo myelination and a drastic drop in brain aspartate (Asp) and N-acetylaspartate (NAA).	N-acetylaspartate	300-303	solute carrier family 25 member 12	Homo sapiens	18-22	
35008954-2	2022	The deficiency in AGC1/Aralar leads to the human rare disease named "early infantile epileptic encephalopathy 39" (EIEE 39, OMIM # 612949) characterized by epilepsy, hypotonia, arrested psychomotor neurodevelopment, hypo myelination and a drastic drop in brain aspartate (Asp) and N-acetylaspartate (NAA).	N-acetylaspartate	300-303	solute carrier family 25 member 12	Homo sapiens	23-29	
35008954-5	2022	Herein, we discuss the role of the AGC1/Aralar-MAS pathway in neuronal functions such as Asp and NAA synthesis, lactate use, respiration on glucose, glutamate (Glu) oxidation and other neurometabolic aspects.	N-acetylaspartate	97-100	solute carrier family 25 member 12	Homo sapiens	35-39	
28235644-0	2017	Down-regulation of the mitochondrial aspartate-glutamate carrier isoform 1 AGC1 inhibits proliferation and N-acetylaspartate synthesis in Neuro2A cells.	N-acetylaspartate	107-124	solute carrier family 25 member 12	Homo sapiens	75-79	
28235644-3	2017	Defects in the AGC1 gene cause AGC1 deficiency, an infantile encephalopathy with delayed myelination and reduced brain N-acetylaspartate (NAA) levels, the precursor of myelin synthesis in the CNS.	N-acetylaspartate	119-136	solute carrier family 25 member 12	Homo sapiens	15-19	
28235644-3	2017	Defects in the AGC1 gene cause AGC1 deficiency, an infantile encephalopathy with delayed myelination and reduced brain N-acetylaspartate (NAA) levels, the precursor of myelin synthesis in the CNS.	N-acetylaspartate	138-141	solute carrier family 25 member 12	Homo sapiens	15-19	
24515575-10	2014	One prior reported SLC25A12 mutation caused complete loss of AGC1 activity in a child with epilepsy, hypotonia, hypomyelination, and reduced brain NAA.	N-acetylaspartate	147-150	solute carrier family 25 member 12	Homo sapiens	61-65	
24515575-12	2014	SLC25A12 sequencing should be considered in children with infantile epilepsy, congenital hypotonia, global delay, abnormal myelination, and reduced brain NAA.	N-acetylaspartate	154-157	solute carrier family 25 member 12	Homo sapiens	0-8