PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 30965084-8 2019 Interestingly, losartan significantly reduced the phosphorylation of Erk1/2 and p38 in Npr1 mice. Losartan 15-23 mitogen-activated protein kinase 3 Mus musculus 69-75 31284709-6 2019 However, galunisertib treatment did not attenuate disrupted medial wall architecture and only partially decreased Erk1/2 phosphorylation, whereas losartan significantly inhibited MFS-associated aortopathy and markedly decreased Erk1/2 phosphorylation in Fbn1C1039G/+ mice. Losartan 146-154 mitogen-activated protein kinase 3 Mus musculus 228-234 30971441-7 2019 We show, in this study, that losartan and its metabolite potently inhibit monocyte recruitment through the noncompetitive inhibition of CCL2-induced ERK1/2 activation, independent of AT1R activity. Losartan 29-37 mitogen-activated protein kinase 3 Mus musculus 149-155 34761239-18 2021 In the BPH/2 and BPN/3 mice with AAA, ERK1/2 activity was significantly increased relative to the respective baseline control (P < .05) and effectively reduced by concomitant Losartan therapy (P < .05). Losartan 175-183 mitogen-activated protein kinase 3 Mus musculus 38-44 34761239-19 2021 Biaxial stretch of the VSMCs in the absence of angiotensin II demonstrated increased ERK1/2 activation (P < .05 vs static control), which was significantly inhibited by Losartan. Losartan 169-177 mitogen-activated protein kinase 3 Mus musculus 85-91 34761239-21 2021 ERK1/2 activity was significantly elevated in the BPH/2 mice and after AAA induction in the normotensive and hypertensive mice but was attenuated by Losartan treatment. Losartan 149-157 mitogen-activated protein kinase 3 Mus musculus 0-6 33145772-0 2021 Cardiac pathology in Mucopolysaccharidosis I mice: Losartan modifies ERK1/2 activation during cardiac remodeling. Losartan 51-59 mitogen-activated protein kinase 3 Mus musculus 69-75 33145772-8 2021 Animals treated with losartan showed a reduction in cathepsin activity and restored ERK1/2 activation. Losartan 21-29 mitogen-activated protein kinase 3 Mus musculus 84-90 25779879-8 2015 At the molecular level, Angiotensin II-induced ERK1/2 phosphorylation in RAW cells was attenuated by Losartan. Losartan 101-109 mitogen-activated protein kinase 3 Mus musculus 47-53 25779879-9 2015 Similarly, RANKL-induced ERK1/2 phosphorylation was suppressed by Losartan, suggesting a convergence of RANKL and angiotensin signaling at the level of ERK1/2 regulation. Losartan 66-74 mitogen-activated protein kinase 3 Mus musculus 152-158 25779879-9 2015 Similarly, RANKL-induced ERK1/2 phosphorylation was suppressed by Losartan, suggesting a convergence of RANKL and angiotensin signaling at the level of ERK1/2 regulation. Losartan 66-74 mitogen-activated protein kinase 3 Mus musculus 25-31 22550139-4 2012 Losartan has been shown to prevent aneurysms in another mouse model of MFS, Fbn1(C1039G/+), through inhibition of the Erk1/2 pathway. Losartan 0-8 mitogen-activated protein kinase 3 Mus musculus 118-124 25122005-6 2014 The increase in ERK1/2 activation by angiotensin-II was blocked by losartan, a blocker of AT1 receptors. Losartan 67-75 mitogen-activated protein kinase 3 Mus musculus 16-22 21109230-11 2011 However, these effects were abolished by pre-treatment with Ang II type 1 (AT1) receptor antagonist, losartan, and the ERK1/2 inhibitor, U0126, inhibited Ang II-mediated IL-6 expression and the phosphorylation of ERK1/2. Losartan 101-109 mitogen-activated protein kinase 3 Mus musculus 213-219 19500499-0 2009 [Losartan inhibits high glucose-induced CTGF expression via ERK1/2 MAPK pathways in mouse mesangial cells]. Losartan 1-9 mitogen-activated protein kinase 3 Mus musculus 60-66 21609620-16 2011 After treated with PRRsiRNA, Losartan or combined therapy, activated ERK1/2 lever was significantly lower than hyperoxia induced group (P < 0.05). Losartan 29-37 mitogen-activated protein kinase 3 Mus musculus 69-75 19500499-9 2009 CONCLUSION: Losartan can inhibit high glucose-induced CTGF expression in mouse mesangial cells, and the mechanisms maybe involve the interruption of ERK1/2 MAPK pathway. Losartan 12-20 mitogen-activated protein kinase 3 Mus musculus 149-155 19500499-7 2009 The protein expression of phosphor-ERK1/2 and CTGF were increased in high glucose group comparing with low glucose group(P<0.01), and reduced in losartan group and ERK inhibitors group comparing with high glucose group(P<0.05). Losartan 148-156 mitogen-activated protein kinase 3 Mus musculus 35-41 18827741-12 2009 Finally, losartan given after sepsis led to inhibition of lung tissue NF-kappaB activation (P < 0.01 vs. CLP group), attenuated degradation of IkappaB-alpha, and inhibited phosphorylation of p38MAPK, extracellular signal-regulated kinase 1/2, and c-Jun N-terminal kinase, pathways critical for cytokine release. Losartan 9-17 mitogen-activated protein kinase 3 Mus musculus 203-273