PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24502696-4	2014	Here we demonstrated that TNF-alpha-induced MMP-9 expression was attenuated by Act.D, CHI, PP1, U0126, SB202190, SP600125, and Bay11-7082, and by the transfection with siRNAs for ERK2, p38 MAPK, and JNK2.	U 0126	96-101	matrix metallopeptidase 9	Mus musculus	44-49	
34169637-5	2021	In addition, blocking ERK1/2 expression with U0126 resulted in the down-regulated expression of CD147, which further led to the decreased expression of MMP-2 and MMP-9.	U 0126	45-50	matrix metallopeptidase 9	Mus musculus	162-167	
29348704-5	2017	Pretreatment with U0126 significantly suppressed phosphorylation of ERK1/2 and further attenuated nicotine-induced activation of c-Jun and upregulation of MMP-2, MMP-9, monocyte chemotactic protein- (MCP-) 1, and regulated upon activation normal T cell expressed and secreted (RANTES).	U 0126	18-23	matrix metallopeptidase 9	Mus musculus	162-167	
24682241-13	2014	Treatment with U0126 inhibited MMP-9 and Bax expression and caspase-3 activation, while it further promoted the expression of the anti-apoptotic molecule Bcl-2, suggesting that resveratrol inhibits MMP-9 expression and cell apoptosis by attenuating the activation of ERK1/2.	U 0126	15-20	matrix metallopeptidase 9	Mus musculus	31-36	
24682241-13	2014	Treatment with U0126 inhibited MMP-9 and Bax expression and caspase-3 activation, while it further promoted the expression of the anti-apoptotic molecule Bcl-2, suggesting that resveratrol inhibits MMP-9 expression and cell apoptosis by attenuating the activation of ERK1/2.	U 0126	15-20	matrix metallopeptidase 9	Mus musculus	198-203	
34099834-5	2021	Treatment with rt-PA demonstrated enhanced MMP-9 protein levels and hemorrhagic transformation which was prevented when U0126 was given in conjunction with rt-PA. By blocking the MMP-9 with U0126 the safety of rt-PA administration was improved and demonstrates a promising adjuvant strategy to reduce the harmful effects of delayed rt-PA treatment in acute ischemic stroke.	U 0126	120-125	matrix metallopeptidase 9	Mus musculus	43-48	
34099834-5	2021	Treatment with rt-PA demonstrated enhanced MMP-9 protein levels and hemorrhagic transformation which was prevented when U0126 was given in conjunction with rt-PA. By blocking the MMP-9 with U0126 the safety of rt-PA administration was improved and demonstrates a promising adjuvant strategy to reduce the harmful effects of delayed rt-PA treatment in acute ischemic stroke.	U 0126	190-195	matrix metallopeptidase 9	Mus musculus	43-48	
34099834-5	2021	Treatment with rt-PA demonstrated enhanced MMP-9 protein levels and hemorrhagic transformation which was prevented when U0126 was given in conjunction with rt-PA. By blocking the MMP-9 with U0126 the safety of rt-PA administration was improved and demonstrates a promising adjuvant strategy to reduce the harmful effects of delayed rt-PA treatment in acute ischemic stroke.	U 0126	190-195	matrix metallopeptidase 9	Mus musculus	179-184	
24502696-7	2014	TNF-alpha time-dependently induced MMP-9 promoter activity which was also inhibited by PP1, U0126, SB202190, SP600125, or Bay11-7082.	U 0126	92-97	matrix metallopeptidase 9	Mus musculus	35-40	
24075781-12	2013	Phosphorylation of ERK1/2 and subsequent secretion of MMP-9 were inhibited by the ERK inhibitor U0126 and not regulated by overexpressed IKKalpha.	U 0126	96-101	matrix metallopeptidase 9	Mus musculus	54-59	
14724072-5	2004	Since mitogen-activated protein kinase ERK1/2 induce MMP-9 expression, we examined whether U0126, an ERK1/2 inhibitor, influenced MMP-9 expression in aged SMC.	U 0126	91-96	matrix metallopeptidase 9	Mus musculus	130-135	
17825046-6	2007	Treatment of mouse embryonic fibroblasts (MEFs) with Con A induces secretion of matrix metalloproteinase (MMP)-9, a phenomenon that is inhibited in cells expressing YF mutant of SHPS-1, a dominant negative form of Akt or in cells pre-treated with an Akt inhibitor, LY294002 or extracellular-signal regulated kinase (Erk) inhibitor, U0126.	U 0126	332-337	matrix metallopeptidase 9	Mus musculus	80-112	
22326785-10	2012	Moreover, U0126, a mitogen-activated protein kinase kinase (MEK) 1/2 inhibitor, and LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor, also inhibited LM8 cell migration, invasion, adhesion, and metastasis, as well as the mRNA expression and protein activities of MMP-1, MMP-2, MMP-9, and MT1-MMP.	U 0126	10-15	matrix metallopeptidase 9	Mus musculus	286-291	
15728252-5	2005	Inhibition of MEK/ERK signaling in wild-type MK cells with a pharmacological inhibitor, U0126, showed that ERK activation was necessary for high levels of endogenous MMP-9 gene expression and activity of a transfected MMP-9 promoter.	U 0126	88-93	matrix metallopeptidase 9	Mus musculus	166-171	
15728252-5	2005	Inhibition of MEK/ERK signaling in wild-type MK cells with a pharmacological inhibitor, U0126, showed that ERK activation was necessary for high levels of endogenous MMP-9 gene expression and activity of a transfected MMP-9 promoter.	U 0126	88-93	matrix metallopeptidase 9	Mus musculus	218-223	
15743030-4	2004	MEK inhibitors (PD98059 and U0126) inhibited the production of MMP-2, MMP-9 and high MW uPA, and upregulated TIMPs (TIMP-1, TIMP-2 and TIMP-3).	U 0126	28-33	matrix metallopeptidase 9	Mus musculus	70-75	
14724072-6	2004	Treatment with U0126 successfully inhibited MMP-9 expression in both young and aged SMC.	U 0126	15-20	matrix metallopeptidase 9	Mus musculus	44-49	
12786942-8	2003	Pretreatment of cells with a MEK1 inhibitor, U0126, also strongly inhibited IL-1beta-dependent secretion of MMP-9.	U 0126	45-50	matrix metallopeptidase 9	Mus musculus	108-113	
12490006-8	2002	U0126 significantly reduced trauma-induced MMP-9 levels.	U 0126	0-5	matrix metallopeptidase 9	Mus musculus	43-48	
12490006-9	2002	Correspondingly, U0126 ameliorated the degradation of the tight junction protein ZO-1, which is an MMP-9 substrate, and significantly attenuated tissue edema.	U 0126	17-22	matrix metallopeptidase 9	Mus musculus	99-104