PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
27190056-4	2016	Impaired FMO3 activity gives rise to the inherited disorder primary trimethylaminuria (TMAU).	Trimethylaminuria	87-91	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	9-13
28196478-1	2017	BACKGROUND: Trimethylaminuria (TMAU) is a genetic disorder whereby people cannot convert trimethylamine (TMA) to its oxidized form (TMAO), a process that requires the liver enzyme FMO3.	Trimethylaminuria	12-29	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	180-184
19577495-8	2009	Analysis of the mutant FMO3 expressed in bacteria revealed that the R238Q mutation abolished catalytic activity of the enzyme and is thus a causative mutation for TMAuria.	Trimethylaminuria	163-170	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	23-27
23791655-1	2013	Trimethylaminuria (TMAu) or "fish odor syndrome" is a metabolic disorder characterized by the inability to convert malodorous dietarily-derived trimethylamine (TMA) to odorless TMA N-oxide by the flavin-containing monooxygenase 3 (FMO3).	Trimethylaminuria	19-23	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	231-235
23266626-3	2013	Several single nucleotide polymorphisms (SNPs) of the FMO3 gene have been described and result in an enzyme with decreased or abolished functional activity for TMA N-oxygenation thus leading to TMAU, or fish-like odor syndrome.	Trimethylaminuria	194-198	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	54-58
23430919-8	2012	The possibility exists that the body odour occasionally associated with betaine therapy for homocystinuria may not be related to increased circulating betaine or DMG, but due to a common FMO3 mutation resulting in TMAU.	Trimethylaminuria	214-218	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	187-191
19321370-4	2009	Several single nucleotide polymorphisms (SNPs) of the FMO3 gene have been described and result in an enzyme with decreased or abolished functional activity for TMA N-oxygenation thus leading to TMAu.	Trimethylaminuria	194-198	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	54-58
19321370-6	2009	Sequence analysis of the exon regions of the FMO3 gene of a young woman with severe TMAu revealed heterozygous mutations at positions 187 (V187A), 158 (E158K), 308 (E308G), and 305 (E305X).	Trimethylaminuria	84-88	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	45-49
19321370-9	2009	Our findings show that with the combination of V187A/E158K mutations in FMO3, the enzyme activity is severely affected and possibly contributes to the TMAu observed.	Trimethylaminuria	151-155	flavin containing dimethylaniline monoxygenase 3	Homo sapiens	72-76