PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24515258-2	2014	The reversible changes in NAA induced by mild TBI were due to a combination of transient mitochondrial malfunctioning with energy crisis (decrease in ATP and in the ATP/ADP ratio) and modulation in the gene and protein levels of N-acetyltransferase 8-like and increase of aspartoacylase levels.	N-acetylaspartate	26-29	N-acetyltransferase 8-like	Rattus norvegicus	229-255	
34573036-1	2021	Neuronal N-acetylaspartate production appears in the presence of aspartate N-acetyltransferase (NAT8L) and binds acetyl groups from acetyl-CoA with aspartic acid.	N-acetylaspartate	9-26	N-acetyltransferase 8-like	Rattus norvegicus	96-101	
32545833-1	2020	N-acetylaspartate is produced by neuronal aspartate N-acetyltransferase (NAT8L) from acetyl-CoA and aspartate.	N-acetylaspartate	0-17	N-acetyltransferase 8-like	Rattus norvegicus	73-78	
24515258-3	2014	The irreversible decrease in NAA following severe TBI, was instead characterized by profound mitochondrial malfunctioning (constant 65% decrease of the ATP/ADP indicating permanent impairment of the mitochondrial phosphorylating capacity), dramatic repression of the N-acetyltransferase 8-like gene and concomitant remarkable increase in the aspartoacylase gene and protein levels.	N-acetylaspartate	29-32	N-acetyltransferase 8-like	Rattus norvegicus	267-293