PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29660387-5 2018 In 12 month-old rats, a long-term treatment with sildenafil (PDE5 inhibitor) normalized testosterone/nitrite levels in circulation and cGMP accumulation in TIF; improved Leydig cell steroidogenic capacity; decreased MEK, ERK1/2 and PRKG1 expression; prevented an increase in the Leydig cells number and atrophy of seminiferous tubules leading to histological appearance of young rat testes. Sildenafil Citrate 49-59 mitogen activated protein kinase 3 Rattus norvegicus 221-227 21325817-13 2011 CONCLUSIONS: 1) Reperfusion injury would result from ROS-triggered MAPK-mediated NHE-1 phosphorylation (and reactivation) during reperfusion; 2) sildenafil protects the myocardium by favouring NHE-1 dephosphorylation and bypassing ROS generation. Sildenafil Citrate 145-155 mitogen activated protein kinase 3 Rattus norvegicus 67-71 25133539-5 2014 Furthermore, sildenafil reduced extracellular signal-regulated kinase (ERK)1/2 and p38 MAPK activation while enhanced activation of the cytoprotective Akt pathway in PH. Sildenafil Citrate 13-23 mitogen activated protein kinase 3 Rattus norvegicus 32-78 23140764-9 2012 In the subacute LVH group, both KMUP-1 and sildenafil administered for 10 days attenuated the LVH in SHRs, with enhanced eNOS/cGMP/PKG and suppressed iNOS/calcineurin A/ERK1/2 expression in the left ventricle. Sildenafil Citrate 43-53 mitogen activated protein kinase 3 Rattus norvegicus 169-175 21948520-6 2012 Sildenafil promoted ERK1/2 activation an effect that was paralleled by an increase in MnSOD expression that persisted 24 hr later. Sildenafil Citrate 0-10 mitogen activated protein kinase 3 Rattus norvegicus 20-26 17898384-9 2007 Sildenafil inhibition of ERK1/2 was accompanied by a rapid induction of MKP-1. Sildenafil Citrate 0-10 mitogen activated protein kinase 3 Rattus norvegicus 25-31 17898384-0 2007 The antiproliferative effect of sildenafil on pulmonary artery smooth muscle cells is mediated via upregulation of mitogen-activated protein kinase phosphatase-1 and degradation of extracellular signal-regulated kinase 1/2 phosphorylation. Sildenafil Citrate 32-42 mitogen activated protein kinase 3 Rattus norvegicus 181-220 17898384-8 2007 Sildenafil (96 microM) also caused a 67% decrease in PDGF-stimulated ERK1/2 phosphorylation. Sildenafil Citrate 0-10 mitogen activated protein kinase 3 Rattus norvegicus 69-75 17898384-11 2007 Either vanadate (12.5 microM), a phosphatase inhibitor, or Rp-8-BrcGMPS abolished the inhibitory effect of sildenafil on PDGF-stimulated phosphorylation of ERK1/2 and restored PDGF-induced cell proliferation. Sildenafil Citrate 107-117 mitogen activated protein kinase 3 Rattus norvegicus 156-162 17898384-12 2007 CONCLUSION: This study indicates that sildenafil upregulates MKP-1 expression and promotes degradation of phosphorylation of ERK1/2, which suppresses the proliferation of pulmonary artery smooth muscle cells. Sildenafil Citrate 38-48 mitogen activated protein kinase 3 Rattus norvegicus 125-131