PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
19622457-0	2009	Azithromycin reduces tumor necrosis factor-alpha production in lipopolysaccharide-stimulated THP-1 monocytic cells by modification of stress response and p38 MAPK pathway.	Azithromycin	0-12	mitogen-activated protein kinase 14	Homo sapiens	154-157	
26655749-9	2016	AZM inhibited the phosphorylation of ERK and p38 MAP kinase in TNF-alpha-stimulated HGEC.	Azithromycin	0-3	mitogen-activated protein kinase 14	Homo sapiens	45-59	
26655749-11	2016	CONCLUSIONS: These results suggested that AZM regulated gingival epithelial permeability through p38 MAP kinase and ERK signaling, and may contribute to suppress the inflammation in gingival tissue.	Azithromycin	42-45	mitogen-activated protein kinase 14	Homo sapiens	97-100	
19622457-4	2009	the results of phosphorylation of three MAPKs, ERK, JNK and p38, indicated that the phospho-p38 level was reduced by AZM.	Azithromycin	117-120	mitogen-activated protein kinase 14	Homo sapiens	60-63	
19622457-4	2009	the results of phosphorylation of three MAPKs, ERK, JNK and p38, indicated that the phospho-p38 level was reduced by AZM.	Azithromycin	117-120	mitogen-activated protein kinase 14	Homo sapiens	92-95	
19622457-8	2009	AZM was found to restrain TNF-alpha production by monocytes at least in part by modifying the HSp-70 and p38 related signaling pathways to LPS stimulation.	Azithromycin	0-3	mitogen-activated protein kinase 14	Homo sapiens	105-108