PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
3265472-5	1988	TPA-treated monocytes exposed to actinomycin D further demonstrated that the half-life of the CSF-1 mRNA is 0.9 h. The results also demonstrated that the protein synthesis inhibitor, cycloheximide (CHX), increases CSF-1 mRNA levels in both resting and TPA-treated monocytes.	Cycloheximide	183-196	colony stimulating factor 1	Homo sapiens	94-99	
3265472-5	1988	TPA-treated monocytes exposed to actinomycin D further demonstrated that the half-life of the CSF-1 mRNA is 0.9 h. The results also demonstrated that the protein synthesis inhibitor, cycloheximide (CHX), increases CSF-1 mRNA levels in both resting and TPA-treated monocytes.	Cycloheximide	183-196	colony stimulating factor 1	Homo sapiens	214-219	
3265472-5	1988	TPA-treated monocytes exposed to actinomycin D further demonstrated that the half-life of the CSF-1 mRNA is 0.9 h. The results also demonstrated that the protein synthesis inhibitor, cycloheximide (CHX), increases CSF-1 mRNA levels in both resting and TPA-treated monocytes.	Cycloheximide	198-201	colony stimulating factor 1	Homo sapiens	94-99	
3265472-7	1988	Moreover, treatment of monocytes with CHX and actinomycin D demonstrated that inhibition of protein synthesis is associated with stabilization of the CSF-1 transcript.	Cycloheximide	38-41	colony stimulating factor 1	Homo sapiens	150-155	
7994042-16	1994	The increase of M-CSF mRNA induction by CHX was 2.5 times higher in cord MNCs compared with that in adult MNCs.	Cycloheximide	40-43	colony stimulating factor 1	Homo sapiens	16-21	
8301137-5	1994	The enhancement of M-CSF message levels in the presence of IL-1 beta was blocked by cycloheximide, suggesting that de novo protein synthesis was required.	Cycloheximide	84-97	colony stimulating factor 1	Homo sapiens	19-24	
8359233-8	1993	We observed, however, that the inhibition of protein synthesis by cycloheximide (CH) in this setting of early monocytic differentiation increased both c-fms and CSF-1 steady-state transcript levels.	Cycloheximide	66-79	colony stimulating factor 1	Homo sapiens	161-166	
8359233-8	1993	We observed, however, that the inhibition of protein synthesis by cycloheximide (CH) in this setting of early monocytic differentiation increased both c-fms and CSF-1 steady-state transcript levels.	Cycloheximide	81-83	colony stimulating factor 1	Homo sapiens	161-166	
7595061-5	1995	Cycloheximide treatment of the cultures containing M-CSF and IFN-gamma inhibited the production of IL-1 beta and TNF-alpha.	Cycloheximide	0-13	colony stimulating factor 1	Homo sapiens	51-56	
8347686-6	1993	Actinomycin D and cycloheximide inhibited both the basal and IL-1 alpha-induced production of M-CSF, suggesting a requirement for de novo RNA and protein synthesis.	Cycloheximide	18-31	colony stimulating factor 1	Homo sapiens	94-99	
2030912-5	1991	Phorbol ester-accelerated processing of the cell surface CSF-1 precursor was abrogated by long-term exposure to phorbol, but was not inhibited by pretreatment with cycloheximide or incubation in serum-free medium.	Cycloheximide	164-177	colony stimulating factor 1	Homo sapiens	57-62	
2105339-4	1990	The combination of a protein synthesis inhibitor, cycloheximide, and TNF increased levels of CSF-1 mRNA compared with treatment by TNF alone.	Cycloheximide	50-63	colony stimulating factor 1	Homo sapiens	93-98