PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29665364-6	2018	Furthermore, casticin significantly prevented the activation of ERK1/2 and NF-kappaB pathways in PDGF-stimulated ASMCs.	asmcs	113-118	mitogen-activated protein kinase 3	Homo sapiens	64-70	
28851074-6	2018	In conclusion, this study demonstrated that MIF overexpression promotes the proliferation and migration of ASMCs by upregulating the activity of the ERK1/2 and FAK signaling pathways in these cells, further indicating that inhibition of MIF may prove to be an effective strategy for treating asthma patients with airway remodeling.	asmcs	107-112	mitogen-activated protein kinase 3	Homo sapiens	149-155	
28081849-9	2017	PDGF-BB significantly increased PRMT1 expression through ERK1/2 MAPK and STAT1 signaling in control ASMCs, whereas in ASMCs from asthmatic patients, these proteins were constitutively expressed.	asmcs	100-105	mitogen-activated protein kinase 3	Homo sapiens	57-63	
28081849-10	2017	ASMCs from asthmatic patients had reduced miR-19a expression, causing upregulation of ERK1/2 MAPK, STAT1, and PRMT1.	asmcs	0-5	mitogen-activated protein kinase 3	Homo sapiens	86-92	
26761017-8	2016	Taken together, oligo-fucoidan supplementation might reduce proliferation of PDGF-treated ASMCs through the suppression of ERK1/2 and Akt phosphorylation and NF-kappaB activation.	asmcs	90-95	mitogen-activated protein kinase 3	Homo sapiens	123-129	
25955575-9	2015	In conclusion, these results indicate that Ang II can induce MMP-2 expression elevation through AT1R and MAPK pathways in ASMCs and suggest that there is therapeutic potential for angiotensin receptor blocker drugs and MAPK inhibitors in the prevention and treatment of ATAAs.	asmcs	122-127	mitogen-activated protein kinase 3	Homo sapiens	105-109	
25955575-9	2015	In conclusion, these results indicate that Ang II can induce MMP-2 expression elevation through AT1R and MAPK pathways in ASMCs and suggest that there is therapeutic potential for angiotensin receptor blocker drugs and MAPK inhibitors in the prevention and treatment of ATAAs.	asmcs	122-127	mitogen-activated protein kinase 3	Homo sapiens	219-223	
22898922-5	2012	IL-17A and IL-17F-induced proliferation of ASMCs was dependent on ERK1/2 MAPK pathway, while IL-22-induced proliferation involved both ERK1/2 MAPK and NF-kappaB pathways.	asmcs	43-48	mitogen-activated protein kinase 3	Homo sapiens	66-72	
23275086-3	2013	We hypotheses that PTEN gene could affect the growth and viability of ASMCs through the regulation of PI3K/Akt, MAPK, and cell cycle-related gene expression.	asmcs	70-75	mitogen-activated protein kinase 3	Homo sapiens	112-116	
22898922-5	2012	IL-17A and IL-17F-induced proliferation of ASMCs was dependent on ERK1/2 MAPK pathway, while IL-22-induced proliferation involved both ERK1/2 MAPK and NF-kappaB pathways.	asmcs	43-48	mitogen-activated protein kinase 3	Homo sapiens	73-77	
21903578-11	2011	We identify that Egr1 (early growth responsive protein-1) activates miR-26a promoter via enhanced phosphorylation of Erk1/2 in ASMCs(Des-/-).	asmcs	127-132	mitogen-activated protein kinase 3	Homo sapiens	117-123	
21903578-13	2011	Moreover, induction of ASMCs(Des-/-) hypertrophy by the Erk-1/2/Egr-1/miR-26a/GSK-3beta pathway is consistent in human recombinant ASMCs, which stably suppresses 90% endogenous desmin expression.	asmcs	23-28	mitogen-activated protein kinase 3	Homo sapiens	56-63	
21903578-13	2011	Moreover, induction of ASMCs(Des-/-) hypertrophy by the Erk-1/2/Egr-1/miR-26a/GSK-3beta pathway is consistent in human recombinant ASMCs, which stably suppresses 90% endogenous desmin expression.	asmcs	131-136	mitogen-activated protein kinase 3	Homo sapiens	56-63	
21493783-8	2011	Moreover, suppressing ERK1/ERK2 activation prevented neutrophil recruitment by ASMCs, whereas suppressing p38 MAPK activity had no impact.	asmcs	79-84	mitogen-activated protein kinase 3	Homo sapiens	22-26