PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33300071-11 2021 PA decreased the production of NO, and the levels of phosphorylated-eNOS, whereas knockdown of CCN1 partially abrogated these effects triggered by PA. Palmitic Acid 0-2 nitric oxide synthase 3 Homo sapiens 68-72 32696742-0 2020 [Palmitic acid decreases phosphorylation of eNOS Ser1177 by activating protein phosphatase 2C (PP2C) of human umbilical vein endothelial cells]. Palmitic Acid 1-14 nitric oxide synthase 3 Homo sapiens 44-48 32696742-1 2020 Objective To investigate the roles of protein phosphatase 2C (PP2C) activated by palmitic acid (PA) in the phosphorylation modulation of endothelial nitric oxide (eNOS) at the site of serine 1177 (eNOS Ser1177) in human umbilical vein endothelial cells (HUVECs). Palmitic Acid 81-94 nitric oxide synthase 3 Homo sapiens 163-167 32696742-1 2020 Objective To investigate the roles of protein phosphatase 2C (PP2C) activated by palmitic acid (PA) in the phosphorylation modulation of endothelial nitric oxide (eNOS) at the site of serine 1177 (eNOS Ser1177) in human umbilical vein endothelial cells (HUVECs). Palmitic Acid 96-98 nitric oxide synthase 3 Homo sapiens 163-167 32696742-1 2020 Objective To investigate the roles of protein phosphatase 2C (PP2C) activated by palmitic acid (PA) in the phosphorylation modulation of endothelial nitric oxide (eNOS) at the site of serine 1177 (eNOS Ser1177) in human umbilical vein endothelial cells (HUVECs). Palmitic Acid 96-98 nitric oxide synthase 3 Homo sapiens 197-201 32696742-6 2020 Results Compared with the control group, the phosphorylation levels of eNOS Ser1177 and NO content decreased significantly in the PA group. Palmitic Acid 130-132 nitric oxide synthase 3 Homo sapiens 71-75 32696742-7 2020 The PP2C inhibitor sanguinarine reversed PA-induced decrease of eNOS Ser1177 phosphorylation level and NO content. Palmitic Acid 41-43 nitric oxide synthase 3 Homo sapiens 64-68 32696742-10 2020 Conclusion PA reduces the phosphorylation level of endothelial eNOS Ser1177 in HUVECs by activating PP2C. Palmitic Acid 11-13 nitric oxide synthase 3 Homo sapiens 63-67 30764838-5 2019 Phosphorylation of Akt and eNOS, as well as NO production were attenuated and accompanied by an increased expression of caspase 3 when HUVECs were subjected to sodium palmitate, and all these changes were restored by pretreatment with U50,488H, the effects of U50,488H were abolished by nor-BNI, and specific inhibitors to PI3K, Akt, eNOS, respectively. Palmitic Acid 160-176 nitric oxide synthase 3 Homo sapiens 334-338 31063772-9 2019 Moreover, treatment of Ea.hy926 cells with palmitic acid or TNFalpha also caused a significant decrease in eNOS activity, which was reversed in iNOS silenced Ea.hy926 cells suggesting the role of iNOS in the reduction of eNOS activity. Palmitic Acid 43-56 nitric oxide synthase 3 Homo sapiens 107-111 31063772-9 2019 Moreover, treatment of Ea.hy926 cells with palmitic acid or TNFalpha also caused a significant decrease in eNOS activity, which was reversed in iNOS silenced Ea.hy926 cells suggesting the role of iNOS in the reduction of eNOS activity. Palmitic Acid 43-56 nitric oxide synthase 3 Homo sapiens 221-225 30764838-5 2019 Phosphorylation of Akt and eNOS, as well as NO production were attenuated and accompanied by an increased expression of caspase 3 when HUVECs were subjected to sodium palmitate, and all these changes were restored by pretreatment with U50,488H, the effects of U50,488H were abolished by nor-BNI, and specific inhibitors to PI3K, Akt, eNOS, respectively. Palmitic Acid 160-176 nitric oxide synthase 3 Homo sapiens 27-31 27665476-14 2016 CONCLUSIONS: Ghrelin pretreatment attenuated LPS- or PA-induced hepatocyte apoptosis, which may least partly via inhibition of mitogen-activated protein kinases (MAPKs)/iNOS and restoration of Akt/eNOS pathways. Palmitic Acid 53-55 nitric oxide synthase 3 Homo sapiens 197-201 25815690-1 2015 Growing evidence suggests that the elevation of free fatty acids, including palmitic acid (PA), are associated with inflammation and oxidative stress, which may be involved in endothelial dysfunction, characterized by the reduced bioavailability of nitric oxide (NO) synthesized from endothelial NO synthase (eNOS). Palmitic Acid 76-89 nitric oxide synthase 3 Homo sapiens 309-313 25815690-7 2015 PA attenuated insulin-mediated insulin receptor substrate-1 (IRS-1) tyrosine phosphorylation, leading to decreased glucose uptake, and phosphorylation of eNOS, leading to a reduction in the production of NO. Palmitic Acid 0-2 nitric oxide synthase 3 Homo sapiens 154-158 25815690-8 2015 Pic effectively mitigated the inhibitory effects of PA on the insulin-mediated phosphorylation of IRS-1 and eNOS, which was not observed following inhibition of HO-1 activity. Palmitic Acid 52-54 nitric oxide synthase 3 Homo sapiens 108-112 25815690-9 2015 The results of the present study suggested that Pic may have the potential to prevent PA-induced impairment of insulin signaling and eNOS function, by inducing the expression of the anti-inflammatory and antioxidant, HO-1. Palmitic Acid 86-88 nitric oxide synthase 3 Homo sapiens 133-137 25815690-1 2015 Growing evidence suggests that the elevation of free fatty acids, including palmitic acid (PA), are associated with inflammation and oxidative stress, which may be involved in endothelial dysfunction, characterized by the reduced bioavailability of nitric oxide (NO) synthesized from endothelial NO synthase (eNOS). Palmitic Acid 91-93 nitric oxide synthase 3 Homo sapiens 309-313 24918290-0 2014 Eicosapentaenoic acid protects against palmitic acid-induced endothelial dysfunction via activation of the AMPK/eNOS pathway. Palmitic Acid 39-52 nitric oxide synthase 3 Homo sapiens 112-116 24918290-6 2014 EPA also restored the PA-mediated reduction of endothelial nitric oxide synthase (eNOS) and AMP-activated protein kinase (AMPK) phosphorylation. Palmitic Acid 1-3 nitric oxide synthase 3 Homo sapiens 47-80 24918290-6 2014 EPA also restored the PA-mediated reduction of endothelial nitric oxide synthase (eNOS) and AMP-activated protein kinase (AMPK) phosphorylation. Palmitic Acid 1-3 nitric oxide synthase 3 Homo sapiens 82-86 24918290-7 2014 Using AMPK siRNA and the specific inhibitor compound C, we found that EPA restored the PA-mediated inhibitions of eNOS and AKT activities via activation of AMPK. Palmitic Acid 71-73 nitric oxide synthase 3 Homo sapiens 114-118 34332276-10 2021 CONCLUSION: Our findings suggest that kappa-OR activation inhibits SP-induced inflammation by activating the PI3K/Akt/eNOS signaling pathway. Palmitic Acid 67-69 nitric oxide synthase 3 Homo sapiens 118-122 19721393-9 2009 CONCLUSIONS: Taken together, we have demonstrated that palmitic acid induces accumulation of ceramide, which appears to mediate palmitic acid"s inhibitory effects on the Akt/eNOS pathway, leading to a significant decrease in NO generation. Palmitic Acid 55-68 nitric oxide synthase 3 Homo sapiens 174-178 19721393-9 2009 CONCLUSIONS: Taken together, we have demonstrated that palmitic acid induces accumulation of ceramide, which appears to mediate palmitic acid"s inhibitory effects on the Akt/eNOS pathway, leading to a significant decrease in NO generation. Palmitic Acid 128-141 nitric oxide synthase 3 Homo sapiens 174-178 34332276-6 2021 RESULTS: The SP-induced hyperlipidemic cell model demonstrated increased expression of NLRP3 and caspase-1 proteins (P < 0.05) and elevated ROS levels (P < 0.01), and decreased phosphorylated-Akt and phosphorylated-eNOS expression (P < 0.05). Palmitic Acid 13-15 nitric oxide synthase 3 Homo sapiens 215-219