PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30525118-1	2018	Objective: Vitamin B6-dependent epilepsies are treatable disorders caused by variants in several genes, such as ALDH7A1,PNPO, and others.	Vitamin B 6	11-21	aldehyde dehydrogenase 7 family member A1	Homo sapiens	112-119	
34138754-2	2021	Bi-allelic ALDH7A1 variants lead to deficiency of alpha-aminoadipic semialdehyde dehydrogenase, resulting in accumulation of piperideine-6-carboxylate (P6C), and secondary deficiency of the important co-factor pyridoxal-5"-phosphate (PLP, active vitamin B6) through its complexation with P6C.	Vitamin B 6	246-256	aldehyde dehydrogenase 7 family member A1	Homo sapiens	11-18	
31741821-1	2019	Vitamin B6-responsive epilepsies are a group of genetic disorders including ALDH7A1 deficiency, PNPO deficiency, and others, usually causing neonatal onset seizures resistant to treatment with common antiepileptic drugs.	Vitamin B 6	0-10	aldehyde dehydrogenase 7 family member A1	Homo sapiens	76-83	
28391250-1	2017	Vitamin-B6-dependent epilepsies are a heterogenous group of treatable disorders due to mutations in several genes (ALDH7A1, PNPO, ALPL or ALDH4A1).	Vitamin B 6	0-10	aldehyde dehydrogenase 7 family member A1	Homo sapiens	115-122	
24114605-1	2014	ALDH7A1 and PNPO deficiencies are rare inborn errors of vitamin B6 metabolism causing perinatal seizure disorders.	Vitamin B 6	56-66	aldehyde dehydrogenase 7 family member A1	Homo sapiens	0-7