PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19727814-10	2010	In addition, our results exhibited that MONCPT obviously down-regulated p-ERK, JNK, p-JNK, and p-p38.	10-methoxy-9-nitrocamptothecin	40-46	mitogen-activated protein kinase 1	Homo sapiens	74-77	
19727814-11	2010	Treatment with p38 mitogen-activated protein kinase (MAPK) SiRNA obviously inhibited p38 MAPK and delayed the G2/M arrest induced by 50.0 nM MONCPT after 48 h. CONCLUSION: Cell cycle regulators, AKT, p53, and MAPK, as therapeutic targets for MONCPT to induce cell cycle G2/M arrest in the context of anticancer therapy.	10-methoxy-9-nitrocamptothecin	242-248	mitogen-activated protein kinase 1	Homo sapiens	89-93	
19727814-11	2010	Treatment with p38 mitogen-activated protein kinase (MAPK) SiRNA obviously inhibited p38 MAPK and delayed the G2/M arrest induced by 50.0 nM MONCPT after 48 h. CONCLUSION: Cell cycle regulators, AKT, p53, and MAPK, as therapeutic targets for MONCPT to induce cell cycle G2/M arrest in the context of anticancer therapy.	10-methoxy-9-nitrocamptothecin	141-147	mitogen-activated protein kinase 1	Homo sapiens	53-57	
19727814-11	2010	Treatment with p38 mitogen-activated protein kinase (MAPK) SiRNA obviously inhibited p38 MAPK and delayed the G2/M arrest induced by 50.0 nM MONCPT after 48 h. CONCLUSION: Cell cycle regulators, AKT, p53, and MAPK, as therapeutic targets for MONCPT to induce cell cycle G2/M arrest in the context of anticancer therapy.	10-methoxy-9-nitrocamptothecin	141-147	mitogen-activated protein kinase 1	Homo sapiens	89-93	
19727814-11	2010	Treatment with p38 mitogen-activated protein kinase (MAPK) SiRNA obviously inhibited p38 MAPK and delayed the G2/M arrest induced by 50.0 nM MONCPT after 48 h. CONCLUSION: Cell cycle regulators, AKT, p53, and MAPK, as therapeutic targets for MONCPT to induce cell cycle G2/M arrest in the context of anticancer therapy.	10-methoxy-9-nitrocamptothecin	242-248	mitogen-activated protein kinase 1	Homo sapiens	53-57