PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 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 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 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 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 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 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 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 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 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 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 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 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