PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 32027883-11 2020 All 20 GSTs mediated the conjugation of GST substrates 1-chloro-2,4-dinitrobenzene; 1,2-epoxy-3-(p-nitrophenoxy)propane; styrene 7,8-oxide; and/or 1-iodohexane, but with different activity levels. amphetaminil 147-159 glutathione S-transferase mu 2 Homo sapiens 7-11 31883408-2 2020 The aim of this study was to investigate the role of farnesoid X receptor (FXR) in 1-deoxysphingolipid de novo synthesis and degradation. amphetaminil 83-102 nuclear receptor subfamily 1, group H, member 4 Mus musculus 53-73 31883408-2 2020 The aim of this study was to investigate the role of farnesoid X receptor (FXR) in 1-deoxysphingolipid de novo synthesis and degradation. amphetaminil 83-102 nuclear receptor subfamily 1, group H, member 4 Mus musculus 75-78 31883408-8 2020 FXR activation by OCA protected the liver against oxidative stress, apoptosis, and reduced 1-deoxysphingolipid levels, both in a HFD-induced mouse model of obesity and in 1-deoxysphinganine-treated mice. amphetaminil 91-110 nuclear receptor subfamily 1, group H, member 4 Mus musculus 0-3 31883408-9 2020 In vitro, FXR activation lowered intracellular 1-deoxysphingolipid levels by inducing Cyp4f -mediated degradation, but not by inhibiting de novo synthesis, thereby protecting hepatocytes against doxSA-induced cytotoxicity, mitochondrial damage, and apoptosis. amphetaminil 47-66 nuclear receptor subfamily 1, group H, member 4 Mus musculus 10-13 31883408-11 2020 Treatment with the Cyp4f pan-inhibitor HET0016 or FXR knockdown fully abolished the protective effect of OCA, indicating that OCA-mediated 1-deoxysphingolipid degradation is FXR- and Cyp4f-dependent. amphetaminil 139-158 nuclear receptor subfamily 1, group H, member 4 Mus musculus 50-53 31883408-11 2020 Treatment with the Cyp4f pan-inhibitor HET0016 or FXR knockdown fully abolished the protective effect of OCA, indicating that OCA-mediated 1-deoxysphingolipid degradation is FXR- and Cyp4f-dependent. amphetaminil 139-158 nuclear receptor subfamily 1, group H, member 4 Mus musculus 174-177 31883408-12 2020 CONCLUSIONS: Our study identifies FXR-Cyp4f as a novel regulatory pathway for 1-deoxysphingolipid metabolism. amphetaminil 78-97 nuclear receptor subfamily 1, group H, member 4 Mus musculus 34-37 31699563-2 2020 Fluorescence analysis showed that 1-OHNap, 9-OHPhe and 1-OHPyr can form 1:1 complex with CAT, with the binding constant of 6.31 x 103, 1.03 x 104 and 2.96 x 105 L mol-1 at 17 C. Thermodynamic and docking parameters demonstrated that van der Waals" force, hydrogen bonds and hydrophobic interactions dominated the three binding processes. amphetaminil 34-41 catalase Homo sapiens 89-92 31699563-2 2020 Fluorescence analysis showed that 1-OHNap, 9-OHPhe and 1-OHPyr can form 1:1 complex with CAT, with the binding constant of 6.31 x 103, 1.03 x 104 and 2.96 x 105 L mol-1 at 17 C. Thermodynamic and docking parameters demonstrated that van der Waals" force, hydrogen bonds and hydrophobic interactions dominated the three binding processes. amphetaminil 55-62 catalase Homo sapiens 89-92 31699563-5 2020 Furthermore, CAT activity was promoted by 9-OHPhe, but inhibited by either 1-OHNap or 1-OHPyr. amphetaminil 75-82 catalase Homo sapiens 13-16 31699563-5 2020 Furthermore, CAT activity was promoted by 9-OHPhe, but inhibited by either 1-OHNap or 1-OHPyr. amphetaminil 86-93 catalase Homo sapiens 13-16 31699563-6 2020 Under the maximum experimental concentration of OH-PAHs, the percent change of CAT activity induced by 1-OHNap, 9-OHPhe and 1-OHPyr were 8.42%, 4.26% and 13.21%. amphetaminil 103-110 catalase Homo sapiens 79-82 31699563-6 2020 Under the maximum experimental concentration of OH-PAHs, the percent change of CAT activity induced by 1-OHNap, 9-OHPhe and 1-OHPyr were 8.42%, 4.26% and 13.21%. amphetaminil 124-131 catalase Homo sapiens 79-82 31780222-2 2020 The formation kinetics of ARP from glycine-ribose system, 3-deoxyribosone (3-DR) and 1-deoxyribosone (1-DR) were evaluated, and then controlled thermal reaction (CTR) coupled with vacuum dehydration was proposed to improve the ARP yield. amphetaminil 85-100 mesencephalic astrocyte derived neurotrophic factor Homo sapiens 26-29 31780222-2 2020 The formation kinetics of ARP from glycine-ribose system, 3-deoxyribosone (3-DR) and 1-deoxyribosone (1-DR) were evaluated, and then controlled thermal reaction (CTR) coupled with vacuum dehydration was proposed to improve the ARP yield. amphetaminil 102-106 mesencephalic astrocyte derived neurotrophic factor Homo sapiens 26-29 32027883-12 2020 Kinetic analyses showed that marmoset GSTM2/GSTM5 and GSTM5/GSTT1 effectively conjugated styrene 7,8-oxide and 1-iodohexane, respectively, with the highest affinity. amphetaminil 111-123 glutathione S-transferase Mu 2 Callithrix jacchus 38-43 32027883-12 2020 Kinetic analyses showed that marmoset GSTM2/GSTM5 and GSTM5/GSTT1 effectively conjugated styrene 7,8-oxide and 1-iodohexane, respectively, with the highest affinity. amphetaminil 111-123 glutathione S-transferase Mu 5 Callithrix jacchus 44-49 32027883-12 2020 Kinetic analyses showed that marmoset GSTM2/GSTM5 and GSTM5/GSTT1 effectively conjugated styrene 7,8-oxide and 1-iodohexane, respectively, with the highest affinity. amphetaminil 111-123 glutathione S-transferase Mu 5 Callithrix jacchus 54-59 32027883-12 2020 Kinetic analyses showed that marmoset GSTM2/GSTM5 and GSTM5/GSTT1 effectively conjugated styrene 7,8-oxide and 1-iodohexane, respectively, with the highest affinity. amphetaminil 111-123 GSTT2B Callithrix jacchus 60-65 31959629-5 2020 The HPK1-mediated AXL degradation was inhibited by the endocytic pathway inhibitors leupeptin, baflomycin A1, and monensin. amphetaminil 95-108 mitogen-activated protein kinase kinase kinase kinase 1 Homo sapiens 4-8 31959629-5 2020 The HPK1-mediated AXL degradation was inhibited by the endocytic pathway inhibitors leupeptin, baflomycin A1, and monensin. amphetaminil 95-108 AXL receptor tyrosine kinase Homo sapiens 18-21 31917923-6 2020 The selective inhibition of the MAO-A and MAO-B isoforms was confirmed ex vivo in mouse brain homogenates, and additional in vivo studies in mice show the therapeutic potential of 1-propargylpiperidines for central nervous system disorders. amphetaminil 180-202 monoamine oxidase A Mus musculus 32-37 31917923-6 2020 The selective inhibition of the MAO-A and MAO-B isoforms was confirmed ex vivo in mouse brain homogenates, and additional in vivo studies in mice show the therapeutic potential of 1-propargylpiperidines for central nervous system disorders. amphetaminil 180-202 monoamine oxidase B Mus musculus 42-47 31560533-4 2019 In the present study we employed a diphosphonate containing a protonated amine, 1-ammoniummethylenediphosphonate [NH3CH(PO3)23-; (Hamdp)], as the ligand to construct paddlewheel Ru2(Hamdp)2 building block. amphetaminil 80-112 doublecortin domain containing 2 Homo sapiens 178-181 31915781-4 2020 1H NMR spectra of 1,1-dinitroethane solution at room temperature in various solvents (carbon tetrachloride, chloroform, dichloromethane, acetone, dimethylformamide and dimethyl sulfoxide) illustrate the increase of 1JCH by several Hz upon an increase of the complex strength. amphetaminil 18-35 joining chain of multimeric IgA and IgM Homo sapiens 216-219 31973006-0 2020 NO1, a New Sigma 2 Receptor/TMEM97 Fluorescent Ligand, Downregulates SOCE and Promotes Apoptosis in the Triple Negative Breast Cancer Cell Lines. amphetaminil 0-3 transmembrane protein 97 Homo sapiens 28-34 31973006-3 2020 The novel sigma2R/TMEM97 fluorescent ligand, NO1, reduced the proliferation and survival of the triple negative breast cancer cell lines (TNBC: MDA-MB-231 and MDA-MB-468 cell lines), due to NO1-induced apoptosis. amphetaminil 45-48 transmembrane protein 97 Homo sapiens 18-24 31973006-3 2020 The novel sigma2R/TMEM97 fluorescent ligand, NO1, reduced the proliferation and survival of the triple negative breast cancer cell lines (TNBC: MDA-MB-231 and MDA-MB-468 cell lines), due to NO1-induced apoptosis. amphetaminil 190-193 transmembrane protein 97 Homo sapiens 18-24 31973006-10 2020 NO1 administration downregulated STIM1-Orai1 interaction, probably by impairing the positive regulatory effect of sigma2R/TMEM97 on STIM1, as we were unable to detect interaction with Orai1. amphetaminil 0-3 stromal interaction molecule 1 Homo sapiens 33-38 31973006-10 2020 NO1 administration downregulated STIM1-Orai1 interaction, probably by impairing the positive regulatory effect of sigma2R/TMEM97 on STIM1, as we were unable to detect interaction with Orai1. amphetaminil 0-3 ORAI calcium release-activated calcium modulator 1 Homo sapiens 39-44 31973006-10 2020 NO1 administration downregulated STIM1-Orai1 interaction, probably by impairing the positive regulatory effect of sigma2R/TMEM97 on STIM1, as we were unable to detect interaction with Orai1. amphetaminil 0-3 transmembrane protein 97 Homo sapiens 122-128 31973006-10 2020 NO1 administration downregulated STIM1-Orai1 interaction, probably by impairing the positive regulatory effect of sigma2R/TMEM97 on STIM1, as we were unable to detect interaction with Orai1. amphetaminil 0-3 stromal interaction molecule 1 Homo sapiens 132-137 31973006-11 2020 (4) Conclusion: sigma2R/TMEM97 is a key protein for the survival of triple negative breast cancer cells by promoting SOCE; therefore, NO1 may become a good pharmacological tool to avoid their proliferation. amphetaminil 134-137 transmembrane protein 97 Homo sapiens 24-30 32055353-3 2019 The approach involves twofold Pd(0)-catalyzed Negishi couplings of 1,1-dibromoalkenes with alkenylzinc reagents, and exploits both substrate- and catalyst-controlled aspects of chemo-, regio- and stereoselectivity in the two C(sp2)-C(sp2) bond forming steps. amphetaminil 67-85 Sp2 transcription factor Homo sapiens 225-230 32055353-3 2019 The approach involves twofold Pd(0)-catalyzed Negishi couplings of 1,1-dibromoalkenes with alkenylzinc reagents, and exploits both substrate- and catalyst-controlled aspects of chemo-, regio- and stereoselectivity in the two C(sp2)-C(sp2) bond forming steps. amphetaminil 67-85 Sp2 transcription factor Homo sapiens 232-237