PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
16099857-7	2005	This possibility was also supported by the finding that the inhibitory effect of c-lact on NE-induced aa-nat induction was markedly reduced by cycloheximide, a protein synthesis inhibitor.	Cycloheximide	143-156	aralkylamine N-acetyltransferase	Rattus norvegicus	102-108	
16887909-10	2006	Early-night administration of cycloheximide actually increased AA-NAT mRNA levels toward the late night.	Cycloheximide	30-43	aralkylamine N-acetyltransferase	Rattus norvegicus	63-69	
17014691-7	2006	In fact, a protein(s) transcribed, later on, as shown by cycloheximide, was responsible for the reversal of the inhibition of Aa-nat transcription.	Cycloheximide	57-70	aralkylamine N-acetyltransferase	Rattus norvegicus	126-132	
16687308-5	2006	Interestingly, injection of the protein synthesis inhibitor cycloheximide before, but not after, the c-FOS/c-JUN peak markedly reduces Aanat mRNA levels.	Cycloheximide	60-73	aralkylamine N-acetyltransferase	Rattus norvegicus	135-140	
178053-2	1976	These effects of choleragen were not blocked by the beta-adrenoceptor antagonist propranolol, but the increases in cyclic adenosine monophosphate phosphodiesterase and serotonin N-acetyltransferase activities could be prevented by the protein synthesis inhibitor cycloheximide.	Cycloheximide	263-276	aralkylamine N-acetyltransferase	Rattus norvegicus	168-197	
4506772-3	1972	Treatment with reserpine, a compound that depletes norepinephrine from nerves, 1-propranolol, a beta-adrenergic blocking agent, or cycloheximide, an inhibitor of protein synthesis, abolishes the nocturnal increase in serotonin N-acetyltransferase activity, indicating that the enzyme activity is modulated by neural release of norepinephrine from sympathetic nerves via beta-adrenergic receptors, and that the increase in enzyme activity is due to synthesis of new enzyme molecules.	Cycloheximide	131-144	aralkylamine N-acetyltransferase	Rattus norvegicus	217-246