PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 33957999-9 2021 Among them, only NPM1-RARA, NUMA-RARA, FIP1L1-RARA, IRF2BP2-RARA, and TFG-RARA have been demonstrated to be sensitive to ATRA, so combined chemotherapy rather than differentiation induction therapy was the standard care for variant APL and these patients would benefit from the quick switch between them. Tretinoin 121-125 factor interacting with PAPOLA and CPSF1 Homo sapiens 39-45 34045202-4 2021 The patient was diagnosed as myeloproliferative neoplasm with a FIP1L1-PDGFRA fusion gene, and successfully treated with the tyrosine kinase inhibitor, imatinib. Imatinib Mesylate 152-160 factor interacting with PAPOLA and CPSF1 Homo sapiens 64-70 34011928-0 2021 Alternative polyadenylation trans-factor FIP1 exacerbates UUO/IRI-induced kidney injury and contributes to AKI-CKD transition via ROS-NLRP3 axis. ros 130-133 factor interacting with PAPOLA and CPSF1 Homo sapiens 41-45 34011928-9 2021 Finally, we proved that FIP1 silencing attenuated the inflammation activation, fibrogenesis, ROS production and apoptosis induced by UUO or IRI. ros 93-96 factor interacting with PAPOLA and CPSF1 Homo sapiens 24-28 33500090-8 2021 The chemically coupled cobalt oxide onto the surface of MWCNTs composite is found highly active towards oxygen evolution reaction (OER) with a low onset potential 1.44 V versus RHE, low overpotential 262 mV at 10 mAcm-2 and small Tafel slope 81 mV dec-1. cobalt oxide 23-35 factor interacting with PAPOLA and CPSF1 Homo sapiens 177-180 34047477-9 2021 Additionally, ZBTB4 bound the MSI promoter region to transcriptionally suppress MSI2 expression, thereby forming an MSI2/SNORD12B/FIP1L1/ZBTB4 feedback loop to regulate the glycolipid metabolism and proliferation of GBM cells. Glycolipids 173-183 factor interacting with PAPOLA and CPSF1 Homo sapiens 130-136 33481974-5 2021 Consequently, Co3O4@NiCo2O4 DSNCs displayed excellent bifunctional electrocatalytic performance, with a positive half-wave potential of 0.81 V (vs. reversible hydrogen electrode, RHE) for ORR (approaching the potential of commercial Pt/C catalyst) and a low potential of 1.65 V at 10 mA cm-2 for OER (exceeding Pt/C). co3o4 14-19 factor interacting with PAPOLA and CPSF1 Homo sapiens 179-182 33637694-12 2021 In general, this study demonstrated that circRAB11FIP1 regulated ATG7 and ATG14 by sponging miR-129. mir-129 92-99 factor interacting with PAPOLA and CPSF1 Homo sapiens 50-54 33481974-5 2021 Consequently, Co3O4@NiCo2O4 DSNCs displayed excellent bifunctional electrocatalytic performance, with a positive half-wave potential of 0.81 V (vs. reversible hydrogen electrode, RHE) for ORR (approaching the potential of commercial Pt/C catalyst) and a low potential of 1.65 V at 10 mA cm-2 for OER (exceeding Pt/C). nico2o4 20-27 factor interacting with PAPOLA and CPSF1 Homo sapiens 179-182 33196011-0 2020 Sustained Complete Molecular Remission With Imatinib Monotherapy in a Child Presenting With Blast Phase FIP1L1-PDGFRA-Associated Myeloid Neoplasm With Eosinophilia. Imatinib Mesylate 44-52 factor interacting with PAPOLA and CPSF1 Homo sapiens 104-110 33445855-0 2020 [Acute myeloid leukemia with FIP1L1-PDGFRA fusion gene treated with imatinib: a case report and literature review]. Imatinib Mesylate 68-76 factor interacting with PAPOLA and CPSF1 Homo sapiens 29-35 32947095-4 2021 Specifically, at the ultrasonic temperature of 35 C, the N-doped MXene (N-MXene-35) exhibits the highest concentration of TiN bond, delivering an extraordinary HER activity with an overpotential of 162 mV (vs. the reversible hydrogen electrode, RHE) at the current density of 10 mA cm-2 in acid media, which is 3.5 times lower than that of the pristine MXene (578 mV vs. RHE). n-doped mxene 58-71 factor interacting with PAPOLA and CPSF1 Homo sapiens 246-249 32947095-4 2021 Specifically, at the ultrasonic temperature of 35 C, the N-doped MXene (N-MXene-35) exhibits the highest concentration of TiN bond, delivering an extraordinary HER activity with an overpotential of 162 mV (vs. the reversible hydrogen electrode, RHE) at the current density of 10 mA cm-2 in acid media, which is 3.5 times lower than that of the pristine MXene (578 mV vs. RHE). n-doped mxene 58-71 factor interacting with PAPOLA and CPSF1 Homo sapiens 372-375 32947095-4 2021 Specifically, at the ultrasonic temperature of 35 C, the N-doped MXene (N-MXene-35) exhibits the highest concentration of TiN bond, delivering an extraordinary HER activity with an overpotential of 162 mV (vs. the reversible hydrogen electrode, RHE) at the current density of 10 mA cm-2 in acid media, which is 3.5 times lower than that of the pristine MXene (578 mV vs. RHE). n-mxene 73-80 factor interacting with PAPOLA and CPSF1 Homo sapiens 246-249 32947095-4 2021 Specifically, at the ultrasonic temperature of 35 C, the N-doped MXene (N-MXene-35) exhibits the highest concentration of TiN bond, delivering an extraordinary HER activity with an overpotential of 162 mV (vs. the reversible hydrogen electrode, RHE) at the current density of 10 mA cm-2 in acid media, which is 3.5 times lower than that of the pristine MXene (578 mV vs. RHE). n-mxene 73-80 factor interacting with PAPOLA and CPSF1 Homo sapiens 372-375 32947095-4 2021 Specifically, at the ultrasonic temperature of 35 C, the N-doped MXene (N-MXene-35) exhibits the highest concentration of TiN bond, delivering an extraordinary HER activity with an overpotential of 162 mV (vs. the reversible hydrogen electrode, RHE) at the current density of 10 mA cm-2 in acid media, which is 3.5 times lower than that of the pristine MXene (578 mV vs. RHE). mxene 66-71 factor interacting with PAPOLA and CPSF1 Homo sapiens 246-249 32947095-4 2021 Specifically, at the ultrasonic temperature of 35 C, the N-doped MXene (N-MXene-35) exhibits the highest concentration of TiN bond, delivering an extraordinary HER activity with an overpotential of 162 mV (vs. the reversible hydrogen electrode, RHE) at the current density of 10 mA cm-2 in acid media, which is 3.5 times lower than that of the pristine MXene (578 mV vs. RHE). mxene 66-71 factor interacting with PAPOLA and CPSF1 Homo sapiens 372-375 32650195-3 2020 We show that the synergistic effect of Fe, N, B in the mesoporous carbon structure can derive excellent ORR activity, for which the FeNB/C-800 catalyst delivers an onset potential of 0.97 V (vs. reversible hydrogen electrode, RHE), a half-wave potential of 0.81 V (vs. RHE) and a high limiting current density (5.59 mA cm-2), comparable to a commercial Pt/C. Iron 39-41 factor interacting with PAPOLA and CPSF1 Homo sapiens 226-229 32929889-5 2020 In alkaline electrolyte, the Co/MnO@N-C presents the outstanding oxygen evolution reaction (OER) performance comparable to the commercial RuO2 catalyst and the exceedingly good oxygen reduction reaction (ORR) activity with positive half-wave potential of 0.90 V vs. RHE outperforming commercial Pt/C (0.84 V vs. RHE) and the recently reported analogous electrocatalysts. Cobalt 29-31 factor interacting with PAPOLA and CPSF1 Homo sapiens 266-269 32929889-5 2020 In alkaline electrolyte, the Co/MnO@N-C presents the outstanding oxygen evolution reaction (OER) performance comparable to the commercial RuO2 catalyst and the exceedingly good oxygen reduction reaction (ORR) activity with positive half-wave potential of 0.90 V vs. RHE outperforming commercial Pt/C (0.84 V vs. RHE) and the recently reported analogous electrocatalysts. Cobalt 29-31 factor interacting with PAPOLA and CPSF1 Homo sapiens 312-315 32929889-5 2020 In alkaline electrolyte, the Co/MnO@N-C presents the outstanding oxygen evolution reaction (OER) performance comparable to the commercial RuO2 catalyst and the exceedingly good oxygen reduction reaction (ORR) activity with positive half-wave potential of 0.90 V vs. RHE outperforming commercial Pt/C (0.84 V vs. RHE) and the recently reported analogous electrocatalysts. mno 32-35 factor interacting with PAPOLA and CPSF1 Homo sapiens 266-269 32929889-5 2020 In alkaline electrolyte, the Co/MnO@N-C presents the outstanding oxygen evolution reaction (OER) performance comparable to the commercial RuO2 catalyst and the exceedingly good oxygen reduction reaction (ORR) activity with positive half-wave potential of 0.90 V vs. RHE outperforming commercial Pt/C (0.84 V vs. RHE) and the recently reported analogous electrocatalysts. mno 32-35 factor interacting with PAPOLA and CPSF1 Homo sapiens 312-315 32929889-5 2020 In alkaline electrolyte, the Co/MnO@N-C presents the outstanding oxygen evolution reaction (OER) performance comparable to the commercial RuO2 catalyst and the exceedingly good oxygen reduction reaction (ORR) activity with positive half-wave potential of 0.90 V vs. RHE outperforming commercial Pt/C (0.84 V vs. RHE) and the recently reported analogous electrocatalysts. Oxygen 65-71 factor interacting with PAPOLA and CPSF1 Homo sapiens 266-269 32929889-5 2020 In alkaline electrolyte, the Co/MnO@N-C presents the outstanding oxygen evolution reaction (OER) performance comparable to the commercial RuO2 catalyst and the exceedingly good oxygen reduction reaction (ORR) activity with positive half-wave potential of 0.90 V vs. RHE outperforming commercial Pt/C (0.84 V vs. RHE) and the recently reported analogous electrocatalysts. Oxygen 65-71 factor interacting with PAPOLA and CPSF1 Homo sapiens 312-315 32650195-3 2020 We show that the synergistic effect of Fe, N, B in the mesoporous carbon structure can derive excellent ORR activity, for which the FeNB/C-800 catalyst delivers an onset potential of 0.97 V (vs. reversible hydrogen electrode, RHE), a half-wave potential of 0.81 V (vs. RHE) and a high limiting current density (5.59 mA cm-2), comparable to a commercial Pt/C. Iron 39-41 factor interacting with PAPOLA and CPSF1 Homo sapiens 269-272 32650195-3 2020 We show that the synergistic effect of Fe, N, B in the mesoporous carbon structure can derive excellent ORR activity, for which the FeNB/C-800 catalyst delivers an onset potential of 0.97 V (vs. reversible hydrogen electrode, RHE), a half-wave potential of 0.81 V (vs. RHE) and a high limiting current density (5.59 mA cm-2), comparable to a commercial Pt/C. Nitrogen 43-44 factor interacting with PAPOLA and CPSF1 Homo sapiens 226-229 32650195-3 2020 We show that the synergistic effect of Fe, N, B in the mesoporous carbon structure can derive excellent ORR activity, for which the FeNB/C-800 catalyst delivers an onset potential of 0.97 V (vs. reversible hydrogen electrode, RHE), a half-wave potential of 0.81 V (vs. RHE) and a high limiting current density (5.59 mA cm-2), comparable to a commercial Pt/C. Nitrogen 43-44 factor interacting with PAPOLA and CPSF1 Homo sapiens 269-272 32650195-3 2020 We show that the synergistic effect of Fe, N, B in the mesoporous carbon structure can derive excellent ORR activity, for which the FeNB/C-800 catalyst delivers an onset potential of 0.97 V (vs. reversible hydrogen electrode, RHE), a half-wave potential of 0.81 V (vs. RHE) and a high limiting current density (5.59 mA cm-2), comparable to a commercial Pt/C. mesoporous 55-65 factor interacting with PAPOLA and CPSF1 Homo sapiens 226-229 32650195-3 2020 We show that the synergistic effect of Fe, N, B in the mesoporous carbon structure can derive excellent ORR activity, for which the FeNB/C-800 catalyst delivers an onset potential of 0.97 V (vs. reversible hydrogen electrode, RHE), a half-wave potential of 0.81 V (vs. RHE) and a high limiting current density (5.59 mA cm-2), comparable to a commercial Pt/C. mesoporous 55-65 factor interacting with PAPOLA and CPSF1 Homo sapiens 269-272 32650195-3 2020 We show that the synergistic effect of Fe, N, B in the mesoporous carbon structure can derive excellent ORR activity, for which the FeNB/C-800 catalyst delivers an onset potential of 0.97 V (vs. reversible hydrogen electrode, RHE), a half-wave potential of 0.81 V (vs. RHE) and a high limiting current density (5.59 mA cm-2), comparable to a commercial Pt/C. Carbon 66-72 factor interacting with PAPOLA and CPSF1 Homo sapiens 226-229 32650195-3 2020 We show that the synergistic effect of Fe, N, B in the mesoporous carbon structure can derive excellent ORR activity, for which the FeNB/C-800 catalyst delivers an onset potential of 0.97 V (vs. reversible hydrogen electrode, RHE), a half-wave potential of 0.81 V (vs. RHE) and a high limiting current density (5.59 mA cm-2), comparable to a commercial Pt/C. Carbon 66-72 factor interacting with PAPOLA and CPSF1 Homo sapiens 269-272 32943629-5 2020 The best CN photoanode demonstrates a benchmark-setting photocurrent density of 353 microA cm-2 (51% faradaic efficiency for oxygen), and external quantum yield value above 12% at 450 nm at 1.23 V versus RHE in an alkaline solution, as well as low onset potential and good stability. photoanode 12-22 factor interacting with PAPOLA and CPSF1 Homo sapiens 204-207 32799460-2 2020 In this work, we report that the metal-organic framework (MOF) indium-based 1,4-benzenedicarboxylate (In-BDC) catalyzes CO2 to formate with a Faradaic efficiency (FEHCOO-) of more than 80% in a wide voltage range between -0.419 and -0.769 V (vs. reversible hydrogen electrode, RHE). Metals 33-38 factor interacting with PAPOLA and CPSF1 Homo sapiens 277-280 32721090-5 2020 In an H-cell system operation at -0.8V vs RHE over 10 h, the current density and FE for CO of Co SAs-Pc dropped by 3.2% and 2.5%. co sas- 94-101 factor interacting with PAPOLA and CPSF1 Homo sapiens 42-45 32721090-5 2020 In an H-cell system operation at -0.8V vs RHE over 10 h, the current density and FE for CO of Co SAs-Pc dropped by 3.2% and 2.5%. CP protocol 101-103 factor interacting with PAPOLA and CPSF1 Homo sapiens 42-45 32430972-2 2020 The photochemical production of H 2 O 2 was achieved at a millimolar level per hour under visible light irradiation along with 100% apparent quantum yield (in 360-450 nm region) and 96% selectivity in an electrochemical system (0.1 V vs. RHE). h 2 o 32-37 factor interacting with PAPOLA and CPSF1 Homo sapiens 238-241 32364409-0 2020 Progressive multifocal leukoencephalopathy responsive to withdrawal of imatinib in a patient with FIP1L1-PDGFRA positive myeloid neoplasm. Imatinib Mesylate 71-79 factor interacting with PAPOLA and CPSF1 Homo sapiens 98-104 32799460-2 2020 In this work, we report that the metal-organic framework (MOF) indium-based 1,4-benzenedicarboxylate (In-BDC) catalyzes CO2 to formate with a Faradaic efficiency (FEHCOO-) of more than 80% in a wide voltage range between -0.419 and -0.769 V (vs. reversible hydrogen electrode, RHE). Indium 63-69 factor interacting with PAPOLA and CPSF1 Homo sapiens 277-280 32799460-2 2020 In this work, we report that the metal-organic framework (MOF) indium-based 1,4-benzenedicarboxylate (In-BDC) catalyzes CO2 to formate with a Faradaic efficiency (FEHCOO-) of more than 80% in a wide voltage range between -0.419 and -0.769 V (vs. reversible hydrogen electrode, RHE). 1,4-benzenedicarboxylate 76-100 factor interacting with PAPOLA and CPSF1 Homo sapiens 277-280 32799460-2 2020 In this work, we report that the metal-organic framework (MOF) indium-based 1,4-benzenedicarboxylate (In-BDC) catalyzes CO2 to formate with a Faradaic efficiency (FEHCOO-) of more than 80% in a wide voltage range between -0.419 and -0.769 V (vs. reversible hydrogen electrode, RHE). Carbon Dioxide 120-123 factor interacting with PAPOLA and CPSF1 Homo sapiens 277-280 32432454-3 2020 This newborn a-NPSB bestows the outstanding catalysis, evidenced by Faradaic efficiency of 88.4% for formate production at -1.15 V vs RHE, and specific current density of 321 mA/mg that is 2 times as that on the Bi nanoparticles. formic acid 101-108 factor interacting with PAPOLA and CPSF1 Homo sapiens 134-137 32195521-4 2020 In a 0.1 M KOH electrolyte, the NH3 yield of the Ru@MXene catalyst reached 2.3 mumol h-1 cm-2, furthermore, at -0.4 V (vs. RHE) the Faraday efficiency was 13.13%. potassium hydroxide 11-14 factor interacting with PAPOLA and CPSF1 Homo sapiens 123-126 32195521-4 2020 In a 0.1 M KOH electrolyte, the NH3 yield of the Ru@MXene catalyst reached 2.3 mumol h-1 cm-2, furthermore, at -0.4 V (vs. RHE) the Faraday efficiency was 13.13%. ru@mxene 49-57 factor interacting with PAPOLA and CPSF1 Homo sapiens 123-126 32125294-0 2020 Exquisite response to imatinib mesylate in FIP1L1-PDGFRA-mutated hypereosinophilic syndrome: a very long-term experience of Polish Hypereosinophilic Syndrome Study Group. Imatinib Mesylate 22-39 factor interacting with PAPOLA and CPSF1 Homo sapiens 43-49 32371867-5 2020 We show that quinone-enriched samples exhibit high selectivity and activity with a H2O2 yield ratio of up to 97.8 % at 0.75 V vs. RHE. quinone 13-20 factor interacting with PAPOLA and CPSF1 Homo sapiens 130-133 32371867-5 2020 We show that quinone-enriched samples exhibit high selectivity and activity with a H2O2 yield ratio of up to 97.8 % at 0.75 V vs. RHE. Hydrogen Peroxide 83-87 factor interacting with PAPOLA and CPSF1 Homo sapiens 130-133 32269633-0 2020 Imatinib therapy in acute myeloid leukemia with DEK-NUP214 and FIP1L1-PDGFRA rearrangement: A case report. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 63-69 32269633-1 2020 The fusion product of FIP1-like-1 (FIP1L1) and platelet-derived growth factor receptor alpha (PDGFRA) gene rearrangement is a tyrosine kinase oncoprotein sensitive to imatinib. Imatinib Mesylate 167-175 factor interacting with PAPOLA and CPSF1 Homo sapiens 22-33 32269633-1 2020 The fusion product of FIP1-like-1 (FIP1L1) and platelet-derived growth factor receptor alpha (PDGFRA) gene rearrangement is a tyrosine kinase oncoprotein sensitive to imatinib. Imatinib Mesylate 167-175 factor interacting with PAPOLA and CPSF1 Homo sapiens 35-41 32079121-3 2020 In this work, we show that N starvation modifies poly(A) usage in a large number of transcripts, some of them mediated by FIP1, a component of the polyadenylation machinery. Nitrogen 27-28 factor interacting with PAPOLA and CPSF1 Homo sapiens 122-126 32154236-8 2020 Among known irritants, high concentrations of methyl violet and methylrosaniline decreased viability, lowered TEER, and increased IL-1alpha secretion in both RhE and FTS models, consistent with irritant properties. Gentian Violet 46-59 factor interacting with PAPOLA and CPSF1 Homo sapiens 158-161 32154236-8 2020 Among known irritants, high concentrations of methyl violet and methylrosaniline decreased viability, lowered TEER, and increased IL-1alpha secretion in both RhE and FTS models, consistent with irritant properties. Gentian Violet 64-80 factor interacting with PAPOLA and CPSF1 Homo sapiens 158-161 32079121-3 2020 In this work, we show that N starvation modifies poly(A) usage in a large number of transcripts, some of them mediated by FIP1, a component of the polyadenylation machinery. Poly A 49-56 factor interacting with PAPOLA and CPSF1 Homo sapiens 122-126 32079121-7 2020 Meta-analyses of APA-affected and fip1-2-deregulated genes indicate a connection between the nitrogen starvation response and salicylic acid (SA) signaling. Nitrogen 93-101 factor interacting with PAPOLA and CPSF1 Homo sapiens 34-38 32079121-7 2020 Meta-analyses of APA-affected and fip1-2-deregulated genes indicate a connection between the nitrogen starvation response and salicylic acid (SA) signaling. Salicylic Acid 126-140 factor interacting with PAPOLA and CPSF1 Homo sapiens 34-38 32079121-7 2020 Meta-analyses of APA-affected and fip1-2-deregulated genes indicate a connection between the nitrogen starvation response and salicylic acid (SA) signaling. Salicylic Acid 142-144 factor interacting with PAPOLA and CPSF1 Homo sapiens 34-38 31914467-8 2020 CONCLUSIONS: In summary, Loeffler"s endocarditis caused by a myeloid and lymphoid neoplasm associated with eosinophilia and abnormalities of FIP1L1-PDGFRA rearrangement could be treated successfully with oral anticoagulation therapy and the tyrosine-kinase inhibitor imatinib. Tyrosine 242-250 factor interacting with PAPOLA and CPSF1 Homo sapiens 142-148 31995156-0 2020 Treatment-free remission in FIP1L1-PDGFRA-positive myeloid/lymphoid neoplasms with eosinophilia after imatinib discontinuation. imatinib 102-110 factor interacting with PAPOLA and CPSF1 Homo sapiens 28-34 31995156-1 2020 FIP1L1-PDGFRA-positive myeloid/lymphoid neoplasms with eosinophilia (MLN-eo) are exquisitely sensitive to imatinib. imatinib 106-114 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 31995156-10 2020 Our data demonstrate that imatinib can be safely stopped in FIP1L1-PDGFRA-positive MLN-eo because of a high treatment-free remission at 12 and 24 months and because most patients achieve a rapid second CMR after restart of imatinib. imatinib 26-34 factor interacting with PAPOLA and CPSF1 Homo sapiens 60-66 31898905-5 2020 Interestingly, it displays a 0.88 V (vs reversible hydrogen electrode, RHE) half-wave potential (E1/2) with a four-electron-transfer pathway and excellent stability outperforming platinum/carbon (Pt/C) in an alkaline medium. Platinum 196-198 factor interacting with PAPOLA and CPSF1 Homo sapiens 71-74 31914467-8 2020 CONCLUSIONS: In summary, Loeffler"s endocarditis caused by a myeloid and lymphoid neoplasm associated with eosinophilia and abnormalities of FIP1L1-PDGFRA rearrangement could be treated successfully with oral anticoagulation therapy and the tyrosine-kinase inhibitor imatinib. imatinib 268-276 factor interacting with PAPOLA and CPSF1 Homo sapiens 142-148 31893229-5 2019 The overpotential of optimized trimetallic Ru38Pd34Ni28 ultrathin NSs is only 20 mV (10 mA cm-2), and the mass activity reaches 6.15 A mg-1 noble metal at -0.07 V vs RHE. nickel-palladium alloy 43-55 factor interacting with PAPOLA and CPSF1 Homo sapiens 166-169 31774621-4 2020 This oxygen-doped complex is used as an effective CO2 catalyst, which exhibits a maximum CO Faradaic efficiency of 91% at -0.8 V (vs reversible hydrogen electrode, RHE) and long-term stability throughout 30 h of electrocatalysis. Oxygen 5-11 factor interacting with PAPOLA and CPSF1 Homo sapiens 164-167 31774621-4 2020 This oxygen-doped complex is used as an effective CO2 catalyst, which exhibits a maximum CO Faradaic efficiency of 91% at -0.8 V (vs reversible hydrogen electrode, RHE) and long-term stability throughout 30 h of electrocatalysis. Carbon Dioxide 50-53 factor interacting with PAPOLA and CPSF1 Homo sapiens 164-167 31774621-4 2020 This oxygen-doped complex is used as an effective CO2 catalyst, which exhibits a maximum CO Faradaic efficiency of 91% at -0.8 V (vs reversible hydrogen electrode, RHE) and long-term stability throughout 30 h of electrocatalysis. Carbon Dioxide 50-52 factor interacting with PAPOLA and CPSF1 Homo sapiens 164-167 31505333-4 2019 The stepwise electrodeposited nickel-iron hydroxide (NiFe(OH)2-SD/NF) electrodes show excellent electrocatalytic activity and stability for the oxygen evolution reaction (OER) with a low potential of 1.45 V (vs RHE) at a current density of 10 mA cm-2. Nickel 30-36 factor interacting with PAPOLA and CPSF1 Homo sapiens 211-214 31867304-3 2019 Compared with the physical mixture of Co3O4 and N-KC and pure N-KC samples, the resulting Co3O4/N-KC nanohybrid afforded remarkably superb ORR activity with a half-wave potential of 0.82 V (vs. reversible hydrogen electrode, RHE) and a limiting current density of 5.70 mA cm-2 in KOH solution (0.1 M). 12-(4'-azido-2'-nitrophenoxy)dodecanoyl-coenzyme A 90-95 factor interacting with PAPOLA and CPSF1 Homo sapiens 225-228 31505333-4 2019 The stepwise electrodeposited nickel-iron hydroxide (NiFe(OH)2-SD/NF) electrodes show excellent electrocatalytic activity and stability for the oxygen evolution reaction (OER) with a low potential of 1.45 V (vs RHE) at a current density of 10 mA cm-2. Ferrous hydroxide 37-51 factor interacting with PAPOLA and CPSF1 Homo sapiens 211-214 31505333-4 2019 The stepwise electrodeposited nickel-iron hydroxide (NiFe(OH)2-SD/NF) electrodes show excellent electrocatalytic activity and stability for the oxygen evolution reaction (OER) with a low potential of 1.45 V (vs RHE) at a current density of 10 mA cm-2. nife(oh)2-sd 53-65 factor interacting with PAPOLA and CPSF1 Homo sapiens 211-214 31505333-5 2019 These electrodes further display excellent catalytic activity towards the urea oxidation reaction (UOR) and hydrazine oxidation reaction (HzOR) with potentials lower than 1.32 V (vs RHE) and 0.06 V (vs RHE), respectively. Urea 74-78 factor interacting with PAPOLA and CPSF1 Homo sapiens 182-185 31505333-5 2019 These electrodes further display excellent catalytic activity towards the urea oxidation reaction (UOR) and hydrazine oxidation reaction (HzOR) with potentials lower than 1.32 V (vs RHE) and 0.06 V (vs RHE), respectively. Urea 74-78 factor interacting with PAPOLA and CPSF1 Homo sapiens 202-205 31505333-5 2019 These electrodes further display excellent catalytic activity towards the urea oxidation reaction (UOR) and hydrazine oxidation reaction (HzOR) with potentials lower than 1.32 V (vs RHE) and 0.06 V (vs RHE), respectively. hydrazine 108-117 factor interacting with PAPOLA and CPSF1 Homo sapiens 182-185 31505333-5 2019 These electrodes further display excellent catalytic activity towards the urea oxidation reaction (UOR) and hydrazine oxidation reaction (HzOR) with potentials lower than 1.32 V (vs RHE) and 0.06 V (vs RHE), respectively. hydrazine 108-117 factor interacting with PAPOLA and CPSF1 Homo sapiens 202-205 31514019-2 2019 Here, we present a collection of 2,6,9-trisubstituted purines with nanomolar potency against PDGFRalpha and strong and selective cytotoxicity in the human eosinophilic leukaemia cell line EOL-1 that expresses the FIP1L1-PDGFRA oncogene. 2,6,9-trisubstituted purines 33-61 factor interacting with PAPOLA and CPSF1 Homo sapiens 213-219 31237394-3 2019 Herein, using on-line differential electrochemical mass spectrometry, we show that oxygen-containing carbon surface groups present on high-surface aera carbon, Vulcan XC72 or reinforced graphite are oxidized at PEMFC anode-relevant potential (E=0.1 V vs. the reversible hydrogen electrode, RHE), but not at E=0.4 V vs. RHE. Oxygen 83-89 factor interacting with PAPOLA and CPSF1 Homo sapiens 290-293 31237394-3 2019 Herein, using on-line differential electrochemical mass spectrometry, we show that oxygen-containing carbon surface groups present on high-surface aera carbon, Vulcan XC72 or reinforced graphite are oxidized at PEMFC anode-relevant potential (E=0.1 V vs. the reversible hydrogen electrode, RHE), but not at E=0.4 V vs. RHE. Oxygen 83-89 factor interacting with PAPOLA and CPSF1 Homo sapiens 319-322 31237394-3 2019 Herein, using on-line differential electrochemical mass spectrometry, we show that oxygen-containing carbon surface groups present on high-surface aera carbon, Vulcan XC72 or reinforced graphite are oxidized at PEMFC anode-relevant potential (E=0.1 V vs. the reversible hydrogen electrode, RHE), but not at E=0.4 V vs. RHE. Carbon 101-107 factor interacting with PAPOLA and CPSF1 Homo sapiens 290-293 31237394-3 2019 Herein, using on-line differential electrochemical mass spectrometry, we show that oxygen-containing carbon surface groups present on high-surface aera carbon, Vulcan XC72 or reinforced graphite are oxidized at PEMFC anode-relevant potential (E=0.1 V vs. the reversible hydrogen electrode, RHE), but not at E=0.4 V vs. RHE. Carbon 101-107 factor interacting with PAPOLA and CPSF1 Homo sapiens 319-322 31237394-3 2019 Herein, using on-line differential electrochemical mass spectrometry, we show that oxygen-containing carbon surface groups present on high-surface aera carbon, Vulcan XC72 or reinforced graphite are oxidized at PEMFC anode-relevant potential (E=0.1 V vs. the reversible hydrogen electrode, RHE), but not at E=0.4 V vs. RHE. Carbon 152-158 factor interacting with PAPOLA and CPSF1 Homo sapiens 290-293 31237394-3 2019 Herein, using on-line differential electrochemical mass spectrometry, we show that oxygen-containing carbon surface groups present on high-surface aera carbon, Vulcan XC72 or reinforced graphite are oxidized at PEMFC anode-relevant potential (E=0.1 V vs. the reversible hydrogen electrode, RHE), but not at E=0.4 V vs. RHE. Carbon 152-158 factor interacting with PAPOLA and CPSF1 Homo sapiens 319-322 31237394-3 2019 Herein, using on-line differential electrochemical mass spectrometry, we show that oxygen-containing carbon surface groups present on high-surface aera carbon, Vulcan XC72 or reinforced graphite are oxidized at PEMFC anode-relevant potential (E=0.1 V vs. the reversible hydrogen electrode, RHE), but not at E=0.4 V vs. RHE. Graphite 186-194 factor interacting with PAPOLA and CPSF1 Homo sapiens 290-293 31237394-3 2019 Herein, using on-line differential electrochemical mass spectrometry, we show that oxygen-containing carbon surface groups present on high-surface aera carbon, Vulcan XC72 or reinforced graphite are oxidized at PEMFC anode-relevant potential (E=0.1 V vs. the reversible hydrogen electrode, RHE), but not at E=0.4 V vs. RHE. Graphite 186-194 factor interacting with PAPOLA and CPSF1 Homo sapiens 319-322 31408825-8 2019 The glucose and lactate concentration in the medium revealed an acute stress reaction of the wounded RHE (wRHE) in the first days after wounding. Glucose 4-11 factor interacting with PAPOLA and CPSF1 Homo sapiens 101-104 31408825-8 2019 The glucose and lactate concentration in the medium revealed an acute stress reaction of the wounded RHE (wRHE) in the first days after wounding. Lactic Acid 16-23 factor interacting with PAPOLA and CPSF1 Homo sapiens 101-104 31198997-5 2019 RESULTS: The incorporation of dermal fibroblasts was sufficient to confer metal sensitivity to RhE. Metals 74-79 factor interacting with PAPOLA and CPSF1 Homo sapiens 95-98 31062583-4 2019 The fabricated WO3/(Er,W):BiVO4 electrode shows photocurrent densities of 4.1 and 7.2 mA cm-2 at 1.23 and 2.3 V (vs reversible hydrogen electrode, RHE), respectively, under a 1 sun illumination in K2HPO4 electrolyte. bismuth vanadium tetraoxide 26-31 factor interacting with PAPOLA and CPSF1 Homo sapiens 147-150 30986374-8 2019 Intriguingly, among several p38 mitogen-activated protein kinase inhibitors, PD169316 alone was able to inhibit growth of T. rubrum on Sabouraud agar and to suppress the process of infection on RHE. 2-(4-nitrophenyl)-4-(4-fluorophenyl)-5-(4-pyridinyl)-1H-imidazole 77-85 factor interacting with PAPOLA and CPSF1 Homo sapiens 194-197 31111599-5 2019 Salt treatment increases the amount of poly(A) site usage within the coding region and 5" untranslated regions (5"-UTRs), and the lack of FIP1 activity reduces the poly(A) site usage within these non-canonical sites. Poly A 164-171 factor interacting with PAPOLA and CPSF1 Homo sapiens 138-142 31111599-7 2019 Root growth assays show that fip1-2 is more tolerant to salt but is hypersensitive to ABA or Cd. Salts 56-60 factor interacting with PAPOLA and CPSF1 Homo sapiens 29-35 31111599-7 2019 Root growth assays show that fip1-2 is more tolerant to salt but is hypersensitive to ABA or Cd. alisol B 23-acetate 86-89 factor interacting with PAPOLA and CPSF1 Homo sapiens 29-35 31111599-7 2019 Root growth assays show that fip1-2 is more tolerant to salt but is hypersensitive to ABA or Cd. Cadmium 93-95 factor interacting with PAPOLA and CPSF1 Homo sapiens 29-35 31021002-5 2019 The FIP1L1-PDGFRA fusion gene (4q12) was detected by fluorescence in situ hybridization and the patient was treated with imatinib mesylate with complete response of the disease. Imatinib Mesylate 121-138 factor interacting with PAPOLA and CPSF1 Homo sapiens 4-10 30807397-0 2019 Myeloid Neoplasm With Eosinophilia and FIP1L1-PDGFRA Rearrangement Treated With Imatinib Mesylate: A Pediatric Case With Long-term Follow-up. Imatinib Mesylate 80-97 factor interacting with PAPOLA and CPSF1 Homo sapiens 39-45 31057777-5 2019 Outstandingly, the catalyst can effectively convert CO2 into CO with a maximum faradaic efficiency of 94.5% and current density of 18.8 mA cm-2 at a low applied potential of -0.60 V (versus reversible hydrogen electrode, RHE). Carbon Dioxide 52-55 factor interacting with PAPOLA and CPSF1 Homo sapiens 221-224 30827111-4 2019 In particular, a strong suppression of HER (below 5% Faradaic efficiency (FE) at -0.8 V vs the reversible hydrogen electrode, RHE) during 20 h was observed. Hydrogen 106-114 factor interacting with PAPOLA and CPSF1 Homo sapiens 126-129 31057777-5 2019 Outstandingly, the catalyst can effectively convert CO2 into CO with a maximum faradaic efficiency of 94.5% and current density of 18.8 mA cm-2 at a low applied potential of -0.60 V (versus reversible hydrogen electrode, RHE). Carbon Monoxide 52-54 factor interacting with PAPOLA and CPSF1 Homo sapiens 221-224 30359545-8 2019 The patient then received imatinib therapy, leading to the complete disappearance of FIP1L1-PDGFRA fusion gene and mutated MYOM2. Imatinib Mesylate 26-34 factor interacting with PAPOLA and CPSF1 Homo sapiens 85-91 31723821-0 2019 FIP1L1-PDGFRalpha p.T674I-D842L: A Novel and Ponatinib Resistant Compound Mutation in FIP1L1-PDGFRalpha Positive Leukemia. ponatinib 45-54 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 31723821-0 2019 FIP1L1-PDGFRalpha p.T674I-D842L: A Novel and Ponatinib Resistant Compound Mutation in FIP1L1-PDGFRalpha Positive Leukemia. ponatinib 45-54 factor interacting with PAPOLA and CPSF1 Homo sapiens 86-92 30444509-1 2018 A new class of 2D fewer-layer pi-conjugated conductive metal-organic nanosheets was developed via the Langmuir-Blodgett method, exhibiting ultrahigh mass activity (64.63 A mg-1, 1.7 V vs. RHE) and stability for electrochemical oxygen evolution reactions (OER). Metals 55-60 factor interacting with PAPOLA and CPSF1 Homo sapiens 188-191 31950612-5 2018 In particular, the Co3 O4 /ZnO hybrid nanostructured electrode (60 s) exhibits the lowest onset potential of 1.5 V (vs. reversible hydrogen electrode, RHE). 12-(4'-azido-2'-nitrophenoxy)dodecanoyl-coenzyme A 19-25 factor interacting with PAPOLA and CPSF1 Homo sapiens 151-154 31950612-5 2018 In particular, the Co3 O4 /ZnO hybrid nanostructured electrode (60 s) exhibits the lowest onset potential of 1.5 V (vs. reversible hydrogen electrode, RHE). Zinc 27-30 factor interacting with PAPOLA and CPSF1 Homo sapiens 151-154 31950612-5 2018 In particular, the Co3 O4 /ZnO hybrid nanostructured electrode (60 s) exhibits the lowest onset potential of 1.5 V (vs. reversible hydrogen electrode, RHE). Hydrogen 131-139 factor interacting with PAPOLA and CPSF1 Homo sapiens 151-154 29079364-4 2018 Twenty eight chemicals including 15 metal salts were topically exposed to RhE. metal salts 36-47 factor interacting with PAPOLA and CPSF1 Homo sapiens 74-77 29691121-5 2018 RESULTS: Both paclitaxel and epothilone B promoted keratinocyte differentiation, accumulation of junctional proteins at the cell cortex, and the early appearance of lamellar bodies in immature RHE, whereas destabilization of microtubules by nocodazole had the reverse effect. Paclitaxel 14-24 factor interacting with PAPOLA and CPSF1 Homo sapiens 193-196 29691121-5 2018 RESULTS: Both paclitaxel and epothilone B promoted keratinocyte differentiation, accumulation of junctional proteins at the cell cortex, and the early appearance of lamellar bodies in immature RHE, whereas destabilization of microtubules by nocodazole had the reverse effect. epothilone B 29-41 factor interacting with PAPOLA and CPSF1 Homo sapiens 193-196 29624891-5 2018 For OERs, the overpotential of Co@N-Carbon at 10 mA cm-2 was 400 mV (vs. reversible hydrogen electrode, RHE). Cobalt 31-33 factor interacting with PAPOLA and CPSF1 Homo sapiens 104-107 29624891-5 2018 For OERs, the overpotential of Co@N-Carbon at 10 mA cm-2 was 400 mV (vs. reversible hydrogen electrode, RHE). Nitrogen 34-35 factor interacting with PAPOLA and CPSF1 Homo sapiens 104-107 29624891-5 2018 For OERs, the overpotential of Co@N-Carbon at 10 mA cm-2 was 400 mV (vs. reversible hydrogen electrode, RHE). Carbon 36-42 factor interacting with PAPOLA and CPSF1 Homo sapiens 104-107 29977537-0 2018 FIP1L1-PDGFRA fusion-negative hypereosinophilic syndrome with uncommon cardiac involvement responding to imatinib treatment: A case report. Imatinib Mesylate 105-113 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 29079364-9 2018 This finding was not related to a lack of stratum corneum skin penetration since EC50 values (decrease in metabolic activity; MTT assay) were obtained after topical RhE exposure to 8 of the 15 metal salts. monooxyethylene trimethylolpropane tristearate 126-129 factor interacting with PAPOLA and CPSF1 Homo sapiens 165-168 30184522-9 2018 That ponatinib briefly induced remission in our patient with acute myeloid leukemia arising from a myeloproliferative neoplasm with eosinophilia and FIP1L1-PDGFRalpha fusion may merit exploration of ponatinib as a potential second-line treatment option for this patient population. ponatinib 5-14 factor interacting with PAPOLA and CPSF1 Homo sapiens 149-155 29276085-6 2018 Importantly, the CFIm activator functions are mediated by the arginine-serine repeat (RS) domains of CFIm68/59, which bind specifically to an RS-like region in the CPSF subunit Fip1, and this interaction is inhibited by CFIm68/59 hyper-phosphorylation. Arginine 62-70 factor interacting with PAPOLA and CPSF1 Homo sapiens 177-181 29276085-6 2018 Importantly, the CFIm activator functions are mediated by the arginine-serine repeat (RS) domains of CFIm68/59, which bind specifically to an RS-like region in the CPSF subunit Fip1, and this interaction is inhibited by CFIm68/59 hyper-phosphorylation. Serine 71-77 factor interacting with PAPOLA and CPSF1 Homo sapiens 177-181 29274231-3 2017 A core CPSF complex comprising CPSF160, WDR33, CPSF30 and Fip1 is sufficient for AAUAAA motif recognition, yet the molecular interactions underpinning its assembly and mechanism of PAS recognition are not understood. Protactinium 181-184 factor interacting with PAPOLA and CPSF1 Homo sapiens 58-62 28742947-3 2017 The dendritic nanostructure of this photoanode with an increased solid-liquid junction area further improves the surface charge collection efficiency, generating a photocurrent of about 2.5 mA cm-2 at 1.23 V versus the reversible hydrogen electrode (vs. RHE) under air mass 1.5G illumination. Hydrogen 230-238 factor interacting with PAPOLA and CPSF1 Homo sapiens 254-257 28742947-4 2017 A photocurrent of approximately 3.1 mA cm-2 at 1.23 V vs. RHE could be achieved by addition of an iron oxide hydroxide cocatalyst. ferric oxyhydroxide 98-118 factor interacting with PAPOLA and CPSF1 Homo sapiens 58-61 28885361-0 2017 Angioimmunoblastic T-cell lymphoma and hypereosinophilic syndrome with FIP1L1/PDGFRA fusion gene effectively treated with imatinib: A case report. Imatinib Mesylate 122-130 factor interacting with PAPOLA and CPSF1 Homo sapiens 71-77 28700953-7 2017 Whilst Ethanol and Propan-2-ol could not be differentiated and displayed good skin tolerance profiles, Propan-1-ol based products lead to significant viability impairments of RhE at 60, 70 or 80% and at 60% in the presence of co-formulates. 1-Propanol 103-114 factor interacting with PAPOLA and CPSF1 Homo sapiens 175-178 28885361-2 2017 Some cases of HES are caused by the FIP1L1/PDGFRA fusion gene and respond to imatinib. Imatinib Mesylate 77-85 factor interacting with PAPOLA and CPSF1 Homo sapiens 36-42 28885361-18 2017 Imatinib was very effective in treating both HES and lymphoma, suggesting that the FIP1L1/PDGFRA fusion gene plays a key role in the pathogenesis of both HES and lymphoma. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 83-89 27760830-7 2017 Indeed, miconazole topically added to RHE was demonstrated to inhibit fungal infection in this model. Miconazole 8-18 factor interacting with PAPOLA and CPSF1 Homo sapiens 38-41 28374041-0 2017 Imatinib Treatment of Lymphomatoid Papulosis Associated with Myeloproliferative Hypereosinophilic Syndrome Presenting the FIP1L1-PDGFRA Fusion Gene. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 122-128 28220996-5 2017 As a result of the nanostructuring and shortened charge collection distance, the nanotube photoanode shows a greatly improved PEC water oxidation activity, exhibiting a photocurrent density of 1.5 mA cm-2 at 1.23 V (vs. reversible hydrogen electrode, RHE), which is the highest among hematite nanotube photoanodes without co-catalysts. Water 130-135 factor interacting with PAPOLA and CPSF1 Homo sapiens 251-254 28253447-6 2017 The onset for As(III) reduction at pH <= 3.5 coincides with the potential for hydrogen electroadsorption on pyrite, E +0.1 V (versus RHE). Hydrogen 81-89 factor interacting with PAPOLA and CPSF1 Homo sapiens 138-141 28253447-6 2017 The onset for As(III) reduction at pH <= 3.5 coincides with the potential for hydrogen electroadsorption on pyrite, E +0.1 V (versus RHE). pyrite 111-117 factor interacting with PAPOLA and CPSF1 Homo sapiens 138-141 28220996-6 2017 Furthermore, a Co-Pi decorated Zr-Fe2 O3 NT photoanode reveals an enhanced onset potential of 0.65 V (vs. RHE) and a photocurrent of 1.87 mA cm-2 (at 1.23 V vs. RHE). zr-fe2 o3 nt photoanode 31-54 factor interacting with PAPOLA and CPSF1 Homo sapiens 106-109 28220996-6 2017 Furthermore, a Co-Pi decorated Zr-Fe2 O3 NT photoanode reveals an enhanced onset potential of 0.65 V (vs. RHE) and a photocurrent of 1.87 mA cm-2 (at 1.23 V vs. RHE). zr-fe2 o3 nt photoanode 31-54 factor interacting with PAPOLA and CPSF1 Homo sapiens 161-164 27911498-3 2017 60 % after 12 h at -0.6 V vs. reversible hydrogen electrode, RHE], and its selectivity was tuned by the introduction of p-block elements (In, Sn, Ga, Al) into the catalyst. Hydrogen 41-49 factor interacting with PAPOLA and CPSF1 Homo sapiens 61-64 30755950-5 2017 LEARNING POINTS: FIP1L1-PDGFRA fusion occurs in 10% of patients with idiopathic hypereosinophilia.Thromboembolism is a known cause of death in hypereosinophilia.The prognosis of FIP1L1-PDGFRA-associated chronic eosinophilic leukemia has been profoundly changed by imatinib treatment. Imatinib Mesylate 264-272 factor interacting with PAPOLA and CPSF1 Homo sapiens 17-23 27911498-7 2017 In contrast, the introduction of Al altered the selectivity profile of the catalyst significantly, decreasing the selectivity toward CO but promoting the reduction of CO2 to ethylene (CE 7 %), n-propanol, and ethanol (CE 2 % each) at -0.8 V vs. RHE. Aluminum 33-35 factor interacting with PAPOLA and CPSF1 Homo sapiens 245-248 27960034-13 2017 Suppression of sumoylation by ginkgolic acid, a small molecule compound inhibiting a SUMO E1-activating enzyme, also destabilizes FIP1L1-PDGFRA, and while the tyrosine kinase inhibitor imatinib suppresses FIP1L1-PDGFRA-dependent cell growth, ginkgolic acid or siRNA of PIAS1 has a synergistic effect with imatinib. ginkgolic acid 30-44 factor interacting with PAPOLA and CPSF1 Homo sapiens 205-211 28186604-10 2017 Imatinib was initiated at a dosage of 200 mg, and after 10 months, the signal of the FIP1L1-PDGFRA fusion gene was undetectable in bone marrow sample. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 85-91 27960034-13 2017 Suppression of sumoylation by ginkgolic acid, a small molecule compound inhibiting a SUMO E1-activating enzyme, also destabilizes FIP1L1-PDGFRA, and while the tyrosine kinase inhibitor imatinib suppresses FIP1L1-PDGFRA-dependent cell growth, ginkgolic acid or siRNA of PIAS1 has a synergistic effect with imatinib. ginkgolic acid 30-44 factor interacting with PAPOLA and CPSF1 Homo sapiens 130-136 27492222-3 2016 We used the model skin sensitizer 2,4-dinitrochlorobenzene (DNCB) to investigate the effects of chemical exposure on GSH lifecycle in reconstructed human epidermis (RHE). Glutathione 117-120 factor interacting with PAPOLA and CPSF1 Homo sapiens 165-168 27831575-2 2016 At the optimal overlayer thickness, the TiO2 nanotube arrays yielded a photocurrent density of up to ~1.75 mA cm-2 at 1.23 V vs. RHE, approximately twice that of the pristine one. titanium dioxide 40-44 factor interacting with PAPOLA and CPSF1 Homo sapiens 129-132 28028904-0 2016 Imatinib-sensitive myeloid neoplasm with low allele burden of FIP1L1-PDGFRA fusion gene in an elderly patient. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 62-68 27492222-4 2016 We demonstrated that the RHE model is suitable to carry out repeated cycles of 2-h exposure to DNCB over a 3-day period. Dinitrochlorobenzene 95-99 factor interacting with PAPOLA and CPSF1 Homo sapiens 25-28 29029406-7 2017 We identified the FIP1L1-PDGFRA/JAK2/Lyn/Akt complex in the F/P-expressing cells which can be disrupted by dual inhibition of JAK2 and Lyn, repressing cell proliferation in both EOL-1(F/P-positive human eosinophilic cell line) and imatinib-resistance (IR) cells. Imatinib Mesylate 231-239 factor interacting with PAPOLA and CPSF1 Homo sapiens 18-24 27711735-4 2016 Ultrathin nanoflakes having a minimized feature size exhibit the best photocurrent of 0.5 mA cm-2 (1.23 V vs. RHE, RHE is reversible hydrogen electrode) among the samples tested as a result of facilitated hole diffusion to the electrolyte and thus lowered carrier recombination. Hydrogen 133-141 factor interacting with PAPOLA and CPSF1 Homo sapiens 110-113 27711735-4 2016 Ultrathin nanoflakes having a minimized feature size exhibit the best photocurrent of 0.5 mA cm-2 (1.23 V vs. RHE, RHE is reversible hydrogen electrode) among the samples tested as a result of facilitated hole diffusion to the electrolyte and thus lowered carrier recombination. Hydrogen 133-141 factor interacting with PAPOLA and CPSF1 Homo sapiens 115-118 27784397-4 2016 CONCLUSION: The proportion of RhD negative donors accounts for 4% of Chinese Nanyang peoples, the RhE/e/C/c types of RhD negative donors are ccdee (50.67%)>Ccdee (33.00%)>ccdEe(5.67%)>CCdee (5.33%)>CcdEe(5.33%). ccdee 141-146 factor interacting with PAPOLA and CPSF1 Homo sapiens 98-101 27784397-4 2016 CONCLUSION: The proportion of RhD negative donors accounts for 4% of Chinese Nanyang peoples, the RhE/e/C/c types of RhD negative donors are ccdee (50.67%)>Ccdee (33.00%)>ccdEe(5.67%)>CCdee (5.33%)>CcdEe(5.33%). ccdee 159-164 factor interacting with PAPOLA and CPSF1 Homo sapiens 98-101 27784397-4 2016 CONCLUSION: The proportion of RhD negative donors accounts for 4% of Chinese Nanyang peoples, the RhE/e/C/c types of RhD negative donors are ccdee (50.67%)>Ccdee (33.00%)>ccdEe(5.67%)>CCdee (5.33%)>CcdEe(5.33%). ccdee 177-182 factor interacting with PAPOLA and CPSF1 Homo sapiens 98-101 27784397-4 2016 CONCLUSION: The proportion of RhD negative donors accounts for 4% of Chinese Nanyang peoples, the RhE/e/C/c types of RhD negative donors are ccdee (50.67%)>Ccdee (33.00%)>ccdEe(5.67%)>CCdee (5.33%)>CcdEe(5.33%). ccdee 193-198 factor interacting with PAPOLA and CPSF1 Homo sapiens 98-101 27784397-4 2016 CONCLUSION: The proportion of RhD negative donors accounts for 4% of Chinese Nanyang peoples, the RhE/e/C/c types of RhD negative donors are ccdee (50.67%)>Ccdee (33.00%)>ccdEe(5.67%)>CCdee (5.33%)>CcdEe(5.33%). ccdee 210-215 factor interacting with PAPOLA and CPSF1 Homo sapiens 98-101 27803915-2 2016 One of the best-characterized forms of HES is the one associated with FIP1L1-PDGFRA gene rearrangement, which was recently demonstrated as responsive to treatment with the small molecule kinase inhibitor drug, imatinib mesylate. Imatinib Mesylate 210-227 factor interacting with PAPOLA and CPSF1 Homo sapiens 70-76 27281158-5 2016 Knowing that reconstructed human epidermis (RHE) models have been demonstrated to be quite similar to the normal human epidermis in terms of metabolic enzymes, use of RHE may be useful to investigate the in situ metabolism/activation of cinnamyl alcohol, particularly when coupled with high-resolution magic angle spinning nuclear magnetic resonance. cinnamyl alcohol 237-253 factor interacting with PAPOLA and CPSF1 Homo sapiens 167-170 27281158-6 2016 Incubation of carbon-13 substituted cinnamyl derivatives with RHE did not result in the formation of cinnamaldehyde. Carbon-13 14-23 factor interacting with PAPOLA and CPSF1 Homo sapiens 62-65 27281158-6 2016 Incubation of carbon-13 substituted cinnamyl derivatives with RHE did not result in the formation of cinnamaldehyde. cinnamyl 36-44 factor interacting with PAPOLA and CPSF1 Homo sapiens 62-65 25431951-0 2014 Antitumor activity of S116836, a novel tyrosine kinase inhibitor, against imatinib-resistant FIP1L1-PDGFRalpha-expressing cells. Imatinib Mesylate 74-82 factor interacting with PAPOLA and CPSF1 Homo sapiens 93-99 27939456-6 2016 However, since early treatment do not reveal impairment to reconstruct a functional epidermal barrier and given the importance of the Th2 dysregulated immune response in AD, cholesterol-depleted RHE at day 11 of reconstruction were then incubated with three Th2-related cytokines (IL-4, IL-13 and IL-25) previously reported as playing important roles in the development of AD, as well as altering overall function of epidermal barrier. Cholesterol 174-185 factor interacting with PAPOLA and CPSF1 Homo sapiens 195-198 26496248-7 2015 Using this technique, we showed that amino acid modifications by this hapten was different according to the model used and that in RHE histidine residues seem to have an important role in the formation of adducts. Histidine 135-144 factor interacting with PAPOLA and CPSF1 Homo sapiens 131-134 25875900-5 2015 In this work, our sandwiched catalyst presents well activities of a low onset of ~1.44 V (vs RHE) and Tafel slope of ~30 mV/decade in 1 M KOH at a scan rate of 5 mV/s. potassium hydroxide 138-141 factor interacting with PAPOLA and CPSF1 Homo sapiens 93-96 25906188-4 2015 Whereas Pcf11 and Fip1 enhance usage of proximal poly(A) sites (pAs), CFI-25/68, PABPN1 and PABPC1 promote usage of distal pAs. Poly A 49-56 factor interacting with PAPOLA and CPSF1 Homo sapiens 18-22 25906188-4 2015 Whereas Pcf11 and Fip1 enhance usage of proximal poly(A) sites (pAs), CFI-25/68, PABPN1 and PABPC1 promote usage of distal pAs. Aminosalicylic Acid 64-67 factor interacting with PAPOLA and CPSF1 Homo sapiens 18-22 25906188-4 2015 Whereas Pcf11 and Fip1 enhance usage of proximal poly(A) sites (pAs), CFI-25/68, PABPN1 and PABPC1 promote usage of distal pAs. Aminosalicylic Acid 123-126 factor interacting with PAPOLA and CPSF1 Homo sapiens 18-22 25906188-5 2015 Strong cis element biases were found for pAs regulated by CFI-25/68 or Fip1, and the distance between pAs plays an important role in APA regulation. Aminosalicylic Acid 41-44 factor interacting with PAPOLA and CPSF1 Homo sapiens 71-75 24576219-0 2015 Newly identified phenotypes in a FIP1L1/PDGFRA-associated paediatric HES patient: thrombocytosis, mHPA, young stroke and blindness. Helium 69-72 factor interacting with PAPOLA and CPSF1 Homo sapiens 33-39 25431951-3 2014 Resistance to imatinib in HES/CEL has been described mainly due to the T674I mutation in FIP1L1-PDGFRalpha, which is homologous to the imatinib-resistant T315I mutation in BCR-ABL. Imatinib Mesylate 14-22 factor interacting with PAPOLA and CPSF1 Homo sapiens 89-95 25431951-3 2014 Resistance to imatinib in HES/CEL has been described mainly due to the T674I mutation in FIP1L1-PDGFRalpha, which is homologous to the imatinib-resistant T315I mutation in BCR-ABL. Imatinib Mesylate 135-143 factor interacting with PAPOLA and CPSF1 Homo sapiens 89-95 27120808-0 2016 Long-term outcomes of imatinib in patients with FIP1L1/ PDGFRA associated chronic eosinophilic leukemia: experience of a single center in China. Imatinib Mesylate 22-30 factor interacting with PAPOLA and CPSF1 Homo sapiens 48-54 27109550-5 2016 Ni4(PET)8 are slightly better catalysts than Ni6(PET)12 which initiate oxygen evolution at an amazingly low overpotential of ~1.51 V (vs. RHE; eta 280 mV). ni4( 0-4 factor interacting with PAPOLA and CPSF1 Homo sapiens 138-141 27109550-5 2016 Ni4(PET)8 are slightly better catalysts than Ni6(PET)12 which initiate oxygen evolution at an amazingly low overpotential of ~1.51 V (vs. RHE; eta 280 mV). ni6(pet)12 45-55 factor interacting with PAPOLA and CPSF1 Homo sapiens 138-141 27109550-5 2016 Ni4(PET)8 are slightly better catalysts than Ni6(PET)12 which initiate oxygen evolution at an amazingly low overpotential of ~1.51 V (vs. RHE; eta 280 mV). Oxygen 71-77 factor interacting with PAPOLA and CPSF1 Homo sapiens 138-141 27109550-6 2016 The peak oxygen evolution current density (J) of ~150 mA cm(-2) at 2.0 V (vs. RHE) with a Tafel slope of 38 mV dec(-1) is observed using Ni4(PET)8. Oxygen 9-15 factor interacting with PAPOLA and CPSF1 Homo sapiens 78-81 26915599-4 2016 The optimized Co@NCN-800 exhibits outstanding HER activity with an onset potential of -89 mV (vs RHE), a large exchange current density of 62.2 muA cm(-2), and small Tafel slope of 82 mV dec(-1), as well as excellent stability (5000 cycles) in acid media, demonstrating the potential for the replacement of Pt-based catalysts. Platinum 307-309 factor interacting with PAPOLA and CPSF1 Homo sapiens 97-100 26757147-4 2016 Then again, pig ear test and MTT assay performed on RHE indicated that gel-like ME is more irritant compared to other tested ME, whereas no difference among formulations were observed by MTT assay on NCTC 2544 cells. methionylglutamic acid 80-82 factor interacting with PAPOLA and CPSF1 Homo sapiens 52-55 26692282-1 2016 Oxide-derived copper (OD-Cu) electrodes exhibit unprecedented CO reduction performance towards liquid fuels, producing ethanol and acetate with >50% Faradaic efficiency at -0.3 V (vs. RHE). Oxides 0-5 factor interacting with PAPOLA and CPSF1 Homo sapiens 187-190 26692282-1 2016 Oxide-derived copper (OD-Cu) electrodes exhibit unprecedented CO reduction performance towards liquid fuels, producing ethanol and acetate with >50% Faradaic efficiency at -0.3 V (vs. RHE). Copper 14-20 factor interacting with PAPOLA and CPSF1 Homo sapiens 187-190 26692282-1 2016 Oxide-derived copper (OD-Cu) electrodes exhibit unprecedented CO reduction performance towards liquid fuels, producing ethanol and acetate with >50% Faradaic efficiency at -0.3 V (vs. RHE). od-cu 22-27 factor interacting with PAPOLA and CPSF1 Homo sapiens 187-190 26692282-3 2016 Acetaldehyde is produced with a Faradaic efficiency of 5% at -0.33 V (vs. RHE). Acetaldehyde 0-12 factor interacting with PAPOLA and CPSF1 Homo sapiens 75-78 26430910-0 2016 Imatinib discontinuation for hypereosinophilic syndrome harboring the FIP1L1-PDGFRA transcript. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 70-76 25761934-2 2015 Imatinib is clinically active in FIP1L1-PDGFRA-positive diseases. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 33-39 25761934-3 2015 Using in vitro screening to identify imatinib-resistant mutations, we frequently detected a Phe to Ser exchange at position 604 (F604S) of FIP1L1-PDGFRA alone or in combination with other exchanges. Imatinib Mesylate 37-45 factor interacting with PAPOLA and CPSF1 Homo sapiens 139-145 25761934-10 2015 Interestingly, FIP1L1-PDGFRA/L629P, a recently identified mutation in an imatinib-resistant CEL patient, also showed protein stabilization similar to that observed with FIP1L1-PDGFRA/F604S. Imatinib Mesylate 73-81 factor interacting with PAPOLA and CPSF1 Homo sapiens 15-21 25589419-7 2015 In addition, selected changes in the expression of several genes suggested that keratinocytes in RHE respond to cholesterol depletion as monolayers. Cholesterol 112-123 factor interacting with PAPOLA and CPSF1 Homo sapiens 97-100 25431951-2 2014 Most FIP1L1-PDGFRalpha-positive patients respond well to the tyrosine kinase inhibitor (TKI) imatinib. Imatinib Mesylate 93-101 factor interacting with PAPOLA and CPSF1 Homo sapiens 5-11 24460680-0 2014 Complete and long-lasting cytologic and molecular remission of FIP1L1-PDGFRA-positive acute eosinophil myeloid leukaemia, treated with low-dose imatinib monotherapy. Imatinib Mesylate 144-152 factor interacting with PAPOLA and CPSF1 Homo sapiens 63-69 24390454-8 2014 Imatinib is a useful adjuvant drug even in PDGRFA/FIP1L1-negative HES. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 50-56 24819164-7 2014 The surface and mass specific activities of the Pt-Y(2)O(3)/C catalyst towards the ORR at 0.9 V (vs. the reversible hydrogen electrode, RHE) are (54.3+-1.2) muA cm(-2)(Pt) and MA=(23.1+-0.5) mA mg(-1)(Pt), respectively. Hydrogen 116-124 factor interacting with PAPOLA and CPSF1 Homo sapiens 136-139 24456122-0 2014 Complete response of monoblastic myeloid sarcoma with FIP1L1- PDGFRA rearrangement to imatinib monotherapy. Imatinib Mesylate 86-94 factor interacting with PAPOLA and CPSF1 Homo sapiens 54-60 24460680-2 2014 The fusion product of such genes is a tyrosine kinase oncoprotein sensitive to imatinib, which to date results to be the standard of care for FIP1L1-PDGFRA-positive chronic myeloproliferative disorders with eosinophilia. Imatinib Mesylate 79-87 factor interacting with PAPOLA and CPSF1 Homo sapiens 142-148 24460680-4 2014 Here, we report a rare case of FIP1L1-PDGFRA-positive acute myeloid leukaemia, with marked peripheral blood and bone marrow eosinophilia, treated with low dose of imatinib monotherapy, achieving a rapid and long-lasting complete cytologic and molecular remission, without need for intensive chemotherapy. Imatinib Mesylate 163-171 factor interacting with PAPOLA and CPSF1 Homo sapiens 31-37 24764730-0 2014 FIP1L1-PDGFRA-Positive Chronic Eosinophilic Leukemia: A Low-Burden Disease with Dramatic Response to Imatinib - A Report of 5 Cases from South India. Imatinib Mesylate 101-109 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 25117044-9 2014 However, the dramatic response to imatinib emphasizes the need to study the presence of the fusion product FIP1L1/PDGFRA in all patients with eosinophilia of unknown etiology. Imatinib Mesylate 34-42 factor interacting with PAPOLA and CPSF1 Homo sapiens 107-113 24407160-0 2014 Identification of Ponatinib as a potent inhibitor of growth, migration, and activation of neoplastic eosinophils carrying FIP1L1-PDGFRA. ponatinib 18-27 factor interacting with PAPOLA and CPSF1 Homo sapiens 122-128 24669761-0 2014 Discovery of imatinib-responsive FIP1L1-PDGFRA mutation during refractory acute myeloid leukemia transformation of chronic myelomonocytic leukemia. Imatinib Mesylate 13-21 factor interacting with PAPOLA and CPSF1 Homo sapiens 33-39 24764730-1 2014 OBJECTIVE: Eosinophilia associated with FIP1L1-PDGFRA rearrangement represents a subset of chronic eosinophilic leukemia and affected patients are sensitive to imatinib treatment. Imatinib Mesylate 160-168 factor interacting with PAPOLA and CPSF1 Homo sapiens 40-46 24302731-6 2014 Knockdown of FIP1/RCP or inhibition of Drp1 markedly impaired mitochondrial remodeling and actin assembly, involving Rab11a-mediated mitochondrial dynamics in E4orf4-induced signaling. e4orf4 159-165 factor interacting with PAPOLA and CPSF1 Homo sapiens 13-17 24009127-0 2014 Cessation of imatinib mesylate may lead to sustained hematologic and molecular remission in FIP1L1-PDGFRA-mutated hypereosinophilic syndrome. Imatinib Mesylate 13-30 factor interacting with PAPOLA and CPSF1 Homo sapiens 92-98 24072151-1 2013 INTRODUCTION: The protective role of recombinant human erythropoietin (RHE) against cisplatin-induced nephrotoxicity has been reported, but the role of sex differences is not clearly known. Cisplatin 84-93 factor interacting with PAPOLA and CPSF1 Homo sapiens 71-74 24156631-1 2013 We report selective electrocatalytic reduction of carbon dioxide to carbon monoxide on gold nanoparticles (NPs) in 0.5 M KHCO3 at 25 C. Among monodisperse 4, 6, 8, and 10 nm NPs tested, the 8 nm Au NPs show the maximum Faradaic efficiency (FE) (up to 90% at -0.67 V vs reversible hydrogen electrode, RHE). Carbon Dioxide 50-64 factor interacting with PAPOLA and CPSF1 Homo sapiens 301-304 24156631-3 2013 This mechanism is further supported by the fact that Au NPs embedded in a matrix of butyl-3-methylimidazolium hexafluorophosphate for more efficient COOH* stabilization exhibit even higher reaction activity (3 A/g mass activity) and selectivity (97% FE) at -0.52 V (vs RHE). Gold 53-55 factor interacting with PAPOLA and CPSF1 Homo sapiens 269-272 24156631-3 2013 This mechanism is further supported by the fact that Au NPs embedded in a matrix of butyl-3-methylimidazolium hexafluorophosphate for more efficient COOH* stabilization exhibit even higher reaction activity (3 A/g mass activity) and selectivity (97% FE) at -0.52 V (vs RHE). butyl-3-methylimidazolium hexafluorophosphate 84-129 factor interacting with PAPOLA and CPSF1 Homo sapiens 269-272 24156631-3 2013 This mechanism is further supported by the fact that Au NPs embedded in a matrix of butyl-3-methylimidazolium hexafluorophosphate for more efficient COOH* stabilization exhibit even higher reaction activity (3 A/g mass activity) and selectivity (97% FE) at -0.52 V (vs RHE). Carbonic Acid 149-153 factor interacting with PAPOLA and CPSF1 Homo sapiens 269-272 24156631-3 2013 This mechanism is further supported by the fact that Au NPs embedded in a matrix of butyl-3-methylimidazolium hexafluorophosphate for more efficient COOH* stabilization exhibit even higher reaction activity (3 A/g mass activity) and selectivity (97% FE) at -0.52 V (vs RHE). Iron 250-252 factor interacting with PAPOLA and CPSF1 Homo sapiens 269-272 24203930-0 2013 Imatinib therapy in a patient with suspected chronic neutrophilic leukemia and FIP1L1-PDGFRA rearrangement. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 79-85 24040321-10 2013 Consistent with its inhibitory role, FIP1 expression was decreased during adipocyte differentiation, by treatment with thiazolidinediones, and with increased BMI in humans. Thiazolidinediones 119-137 factor interacting with PAPOLA and CPSF1 Homo sapiens 37-41 24072151-2 2013 The aim of this study was to determine the sex-based difference in the protective effect of RHE against cisplatin-induced nephrotoxicity. Cisplatin 104-113 factor interacting with PAPOLA and CPSF1 Homo sapiens 92-95 24072151-11 2013 Administration of RHE significantly decreased changes in serum creatinine, BUN, and malondialdehyde levels in male rats, but not in females. Creatinine 63-73 factor interacting with PAPOLA and CPSF1 Homo sapiens 18-21 24072151-11 2013 Administration of RHE significantly decreased changes in serum creatinine, BUN, and malondialdehyde levels in male rats, but not in females. Malondialdehyde 84-99 factor interacting with PAPOLA and CPSF1 Homo sapiens 18-21 23256819-5 2013 Thus, while the modification of proteins or peptides in solution takes several days to lead to a significant amount of modification, in RHE the modifications of nucleophilic amino acids were observable already at 24 h. The chemioselectivity also appeared to be different with major modifications taking place on histidine, methionine, and cysteine residues in RHE, while on HSA, significant modifications were observed on lysine residues with the formation of methylated and dimethylated amino groups. Histidine 312-321 factor interacting with PAPOLA and CPSF1 Homo sapiens 136-139 23201050-4 2013 We have compared the esteratic cleavage of the prednisolone diester prednicarbate and the enzyme kinetic parameters (Vmax and S0.5) of the model substrate fluorescein diacetate (FDA) in commercially available RHS and RHE with excised human skin and monolayer cultures of normal and immortalised human keratinocytes and of fibroblasts. diacetylfluorescein 178-181 factor interacting with PAPOLA and CPSF1 Homo sapiens 217-220 23201050-5 2013 Formation of the main metabolite prednisolone and of fluorescein ranked as: RHS~RHE>excised human skin and keratinocytes>fibroblasts, respectively. Prednisolone 33-45 factor interacting with PAPOLA and CPSF1 Homo sapiens 80-83 23201050-5 2013 Formation of the main metabolite prednisolone and of fluorescein ranked as: RHS~RHE>excised human skin and keratinocytes>fibroblasts, respectively. Fluorescein 53-64 factor interacting with PAPOLA and CPSF1 Homo sapiens 80-83 23611226-0 2013 [FIP1L1-PDGFRA positive chronic eosinophilic leukemia with imatinib-resistant T674I mutant of PDGFRA gene: a case report and literature review]. Imatinib Mesylate 59-67 factor interacting with PAPOLA and CPSF1 Homo sapiens 1-7 23982058-1 2013 Imatinib is the treatment of choice for FIP1L1/PDGFRA (F/P)-associated chronic eosinophilic leukemia (F/P CEL), but its optimal dosing, duration, and possibility of discontinuation are still a matter of debate. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 40-46 23157309-0 2013 Sorafenib is effective for imatinib-resistant FIP1L1/PDGFRA T674I mutation-positive acute myeloid leukemia with eosinophilia. Sorafenib 0-9 factor interacting with PAPOLA and CPSF1 Homo sapiens 46-52 23157309-0 2013 Sorafenib is effective for imatinib-resistant FIP1L1/PDGFRA T674I mutation-positive acute myeloid leukemia with eosinophilia. Imatinib Mesylate 27-35 factor interacting with PAPOLA and CPSF1 Homo sapiens 46-52 23256819-5 2013 Thus, while the modification of proteins or peptides in solution takes several days to lead to a significant amount of modification, in RHE the modifications of nucleophilic amino acids were observable already at 24 h. The chemioselectivity also appeared to be different with major modifications taking place on histidine, methionine, and cysteine residues in RHE, while on HSA, significant modifications were observed on lysine residues with the formation of methylated and dimethylated amino groups. Methionine 323-333 factor interacting with PAPOLA and CPSF1 Homo sapiens 136-139 23256819-5 2013 Thus, while the modification of proteins or peptides in solution takes several days to lead to a significant amount of modification, in RHE the modifications of nucleophilic amino acids were observable already at 24 h. The chemioselectivity also appeared to be different with major modifications taking place on histidine, methionine, and cysteine residues in RHE, while on HSA, significant modifications were observed on lysine residues with the formation of methylated and dimethylated amino groups. Cysteine 339-347 factor interacting with PAPOLA and CPSF1 Homo sapiens 136-139 23256819-5 2013 Thus, while the modification of proteins or peptides in solution takes several days to lead to a significant amount of modification, in RHE the modifications of nucleophilic amino acids were observable already at 24 h. The chemioselectivity also appeared to be different with major modifications taking place on histidine, methionine, and cysteine residues in RHE, while on HSA, significant modifications were observed on lysine residues with the formation of methylated and dimethylated amino groups. Lysine 422-428 factor interacting with PAPOLA and CPSF1 Homo sapiens 136-139 22806436-11 2012 Using of low-dose imatinib mesylate (100 mg/day) a hematological and molecular remission in all patients displaying the FIP1L1-PDGFRA fusion gene was observed. Imatinib Mesylate 18-35 factor interacting with PAPOLA and CPSF1 Homo sapiens 120-126 23151016-3 2012 A Co-/Fe-coordinating pyrolyzed polymer exhibited a high specific oxygen reduction activity with onset and half-wave potentials of 0.87 and 0.76 V vs RHE, respectively, in neutral media. Iron 6-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 150-153 23151016-3 2012 A Co-/Fe-coordinating pyrolyzed polymer exhibited a high specific oxygen reduction activity with onset and half-wave potentials of 0.87 and 0.76 V vs RHE, respectively, in neutral media. Oxygen 66-72 factor interacting with PAPOLA and CPSF1 Homo sapiens 150-153 21258876-0 2012 Imatinib mesylate may induce long-term clinical response in FIP1L1-PDGFRalpha-negative hypereosinophilic syndrome. Imatinib Mesylate 0-17 factor interacting with PAPOLA and CPSF1 Homo sapiens 60-66 22271894-9 2012 Nuclear factor-kappaB was also activated in the human FIP1L1-PDGFRA-positive leukemia cell line EOL1, the proliferation of which was blocked by bortezomib and the IkappaB kinase inhibitor BMS-345541. Bortezomib 144-154 factor interacting with PAPOLA and CPSF1 Homo sapiens 54-60 22301675-0 2012 Ponatinib is active against imatinib-resistant mutants of FIP1L1-PDGFRA and KIT, and against FGFR1-derived fusion kinases. ponatinib 0-9 factor interacting with PAPOLA and CPSF1 Homo sapiens 58-64 22616945-6 2012 Peak CO(2) conversion occurred at -1 V (vs RHE) with approximately 100% efficiency and a rate 7-700 times higher than that for larger Au catalysts and 10-100 times higher than those for current state-of-the-art processes. co(2) 5-10 factor interacting with PAPOLA and CPSF1 Homo sapiens 43-46 22769428-5 2012 Compared with N-doped carbon, B,N-doped or P,N-doped carbon shows 1.2 or 2.1 times higher ORR activity at 0.6 V (vs RHE) in acidic media. Carbon 53-59 factor interacting with PAPOLA and CPSF1 Homo sapiens 116-119 22769428-6 2012 The most active catalyst in the reaction is the ternary-doped carbon (B,P,N-doped carbon), which records -6.0 mA/mg of mass activity at 0.6 V (vs RHE), and it is 2.3 times higher than that of the N-doped carbon. Carbon 62-68 factor interacting with PAPOLA and CPSF1 Homo sapiens 146-149 22769428-6 2012 The most active catalyst in the reaction is the ternary-doped carbon (B,P,N-doped carbon), which records -6.0 mA/mg of mass activity at 0.6 V (vs RHE), and it is 2.3 times higher than that of the N-doped carbon. Carbon 82-88 factor interacting with PAPOLA and CPSF1 Homo sapiens 146-149 22769428-6 2012 The most active catalyst in the reaction is the ternary-doped carbon (B,P,N-doped carbon), which records -6.0 mA/mg of mass activity at 0.6 V (vs RHE), and it is 2.3 times higher than that of the N-doped carbon. Carbon 82-88 factor interacting with PAPOLA and CPSF1 Homo sapiens 146-149 22301675-0 2012 Ponatinib is active against imatinib-resistant mutants of FIP1L1-PDGFRA and KIT, and against FGFR1-derived fusion kinases. Imatinib Mesylate 28-36 factor interacting with PAPOLA and CPSF1 Homo sapiens 58-64 21258876-2 2012 Eight patients with a median age at diagnosis of 42 years (range 19-67) received imatinib mesylate (IM) for FIP1L1-PDGFRalpha-negative HES resistant to previous conventional treatment. Imatinib Mesylate 81-98 factor interacting with PAPOLA and CPSF1 Homo sapiens 108-114 22407419-3 2012 High performance was observed for the alpha-Ni(0.87)Zn(0.13) and beta(1)-Ni(0.50)Zn(0.50) electrocatalysts with an onset potential of -0.15 V (vs. RHE) and a mass activity of 4000-3800 A g(cat)(-1) at 0.4 V (vs. RHE), respectively. alpha-ni 38-46 factor interacting with PAPOLA and CPSF1 Homo sapiens 147-150 22407419-3 2012 High performance was observed for the alpha-Ni(0.87)Zn(0.13) and beta(1)-Ni(0.50)Zn(0.50) electrocatalysts with an onset potential of -0.15 V (vs. RHE) and a mass activity of 4000-3800 A g(cat)(-1) at 0.4 V (vs. RHE), respectively. beta(1)-ni 65-75 factor interacting with PAPOLA and CPSF1 Homo sapiens 147-150 22407419-3 2012 High performance was observed for the alpha-Ni(0.87)Zn(0.13) and beta(1)-Ni(0.50)Zn(0.50) electrocatalysts with an onset potential of -0.15 V (vs. RHE) and a mass activity of 4000-3800 A g(cat)(-1) at 0.4 V (vs. RHE), respectively. alpha-ni 38-46 factor interacting with PAPOLA and CPSF1 Homo sapiens 212-215 22407419-3 2012 High performance was observed for the alpha-Ni(0.87)Zn(0.13) and beta(1)-Ni(0.50)Zn(0.50) electrocatalysts with an onset potential of -0.15 V (vs. RHE) and a mass activity of 4000-3800 A g(cat)(-1) at 0.4 V (vs. RHE), respectively. beta(1)-ni 65-75 factor interacting with PAPOLA and CPSF1 Homo sapiens 212-215 22281951-2 2012 The theoretical free energy diagram indicates that sulfuric acid anions adsorb as bisulfate in the potential range of 0.41 < U <= 0.48 V (RHE) and as sulfate in 0.48 V (RHE) < U. sulfuric acid 51-64 factor interacting with PAPOLA and CPSF1 Homo sapiens 144-147 22281951-2 2012 The theoretical free energy diagram indicates that sulfuric acid anions adsorb as bisulfate in the potential range of 0.41 < U <= 0.48 V (RHE) and as sulfate in 0.48 V (RHE) < U. sulfuric acid 51-64 factor interacting with PAPOLA and CPSF1 Homo sapiens 175-178 22281951-2 2012 The theoretical free energy diagram indicates that sulfuric acid anions adsorb as bisulfate in the potential range of 0.41 < U <= 0.48 V (RHE) and as sulfate in 0.48 V (RHE) < U. hydrogen sulfate 82-91 factor interacting with PAPOLA and CPSF1 Homo sapiens 144-147 22281951-2 2012 The theoretical free energy diagram indicates that sulfuric acid anions adsorb as bisulfate in the potential range of 0.41 < U <= 0.48 V (RHE) and as sulfate in 0.48 V (RHE) < U. Sulfates 84-91 factor interacting with PAPOLA and CPSF1 Homo sapiens 144-147 22281951-2 2012 The theoretical free energy diagram indicates that sulfuric acid anions adsorb as bisulfate in the potential range of 0.41 < U <= 0.48 V (RHE) and as sulfate in 0.48 V (RHE) < U. Sulfates 84-91 factor interacting with PAPOLA and CPSF1 Homo sapiens 175-178 22281951-4 2012 Charge analysis shows that the total charge transferred for the formation of the full coverage sulfate adlayer is 90 muC cm(-2), and that the electrosorption valency value is -0.45 to -0.95 in 0.41 < U <= 0.48 V (RHE) and -1.75 to -1.85 in U > 0.48 V (RHE) in good agreement with experiments reported in the literature. Sulfates 95-102 factor interacting with PAPOLA and CPSF1 Homo sapiens 219-222 22281951-4 2012 Charge analysis shows that the total charge transferred for the formation of the full coverage sulfate adlayer is 90 muC cm(-2), and that the electrosorption valency value is -0.45 to -0.95 in 0.41 < U <= 0.48 V (RHE) and -1.75 to -1.85 in U > 0.48 V (RHE) in good agreement with experiments reported in the literature. Sulfates 95-102 factor interacting with PAPOLA and CPSF1 Homo sapiens 261-264 21818111-0 2012 Limited clinical activity of nilotinib and sorafenib in FIP1L1-PDGFRA positive chronic eosinophilic leukemia with imatinib-resistant T674I mutation. Sorafenib 43-52 factor interacting with PAPOLA and CPSF1 Homo sapiens 56-62 22722648-0 2012 Complete response of myeloid sarcoma with FIP1L1-PDGFRA -associated myeloproliferative neoplasms to imatinib mesylate monotherapy. Imatinib Mesylate 100-117 factor interacting with PAPOLA and CPSF1 Homo sapiens 42-48 22829096-3 2011 Real-time reverse transcription PCR found that long-term exposure of chronic eosinophilic leukemia EOL-1 cells expressing FIP1L1/platelet-derived growth factor receptor-alpha to imatinib induced expression of DNA methyltransferase 3A (DNMT3A) and histone-methyltransferase enhancer of zeste homolog 2 (EZH2), a family of polycomb group, thereby increasing methylation of the gene. Imatinib Mesylate 178-186 factor interacting with PAPOLA and CPSF1 Homo sapiens 122-128 22975968-1 2012 The skin irritation test is designed for the prediction of acute skin irritation of nanoparticles by measurement of its cytotoxic effect, as reflected in the MTT assay, on the Reconstructed Human Epidermis (RHE) model. monooxyethylene trimethylolpropane tristearate 158-161 factor interacting with PAPOLA and CPSF1 Homo sapiens 207-210 22348015-5 2012 The new model system is feasible for the evaluation of new tyrosine kinase inhibitors and our data suggest that nilotinib may be a valuable additional targeted drug active in patients with FIP1L1/PDGFRA+ CEL. nilotinib 112-121 factor interacting with PAPOLA and CPSF1 Homo sapiens 189-195 21924129-0 2011 [Durable efficacity and remission after treatment with imatinib mesylate for FIP1L1-PDGFRA transcript negative associated eosinophilic cardiomyopathy]. Imatinib Mesylate 55-72 factor interacting with PAPOLA and CPSF1 Homo sapiens 77-83 22204765-4 2011 These findings have been quite significant, as those individuals with a FIP1L1-PDGFRA fusion have an exquisite susceptibility to tyrosine kinase inhibitors (TKIs), such as imatinib mesylate. Imatinib Mesylate 172-189 factor interacting with PAPOLA and CPSF1 Homo sapiens 72-78 20609486-0 2011 Complete reversal of left ventricular mass in FIP1L1-PDGFRA-positive chronic eosinophilic leukemia after therapy with imatinib. Imatinib Mesylate 118-126 factor interacting with PAPOLA and CPSF1 Homo sapiens 46-52 21924129-3 2011 Since the discovery of the involvement of deregulated tyrosine kinases in the pathophysiology of these diseases, and particularly the identification of the fusion gene FIP1L1-PDGFRA, new molecules inhibiting specifically this signaling pathway (imatinib) were individualized, leading to dramatic therapeutic benefits in proliferative forms of HES considered before that of very poor prognosis. Imatinib Mesylate 245-253 factor interacting with PAPOLA and CPSF1 Homo sapiens 168-174 21924129-4 2011 CASE REPORT: We report here the dramatic effectiveness of imatinib used as second line therapy for dilated cardiomyopathy revealing a hypereosinophilic syndrome in a patient in whom the search for FIP1-L1-PDGFRA fusion gene was negative. Imatinib Mesylate 58-66 factor interacting with PAPOLA and CPSF1 Homo sapiens 197-204 21924129-6 2011 We report here a case of HES lacking the FIP1-L1-PDGFRA fusion gene showing that despite the absence of this molecular defect, imatinib mesylate may have therapeutic interest in those cases of HES resistant to first line therapies. Imatinib Mesylate 127-144 factor interacting with PAPOLA and CPSF1 Homo sapiens 41-48 21463117-7 2011 Imatinib has been used successfully to treat patients with chronic eosinophilic disorders with the FIP1L1-PDGFRA fusion kinase; limited clinical data indicate that dasatinib could be active in imatinib-resistant disease. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 99-105 21152975-2 2011 Subsequently it was found to have multiple functions and regulate the activity of diverse proteins, including regulation of HCO(3)(-) transporters to coordinate epithelial HCO(3)(-) secretion and to determine localization of the Fip1 subunit of the CPSF complex to regulate mRNA processing. Bicarbonates 124-130 factor interacting with PAPOLA and CPSF1 Homo sapiens 229-233 21821988-9 2011 The peak level (Cmax) of dasatinib in this patient was 55.3 nM, which exceeded the concentration of dasatinib required to inhibit cells with FIP1L1-PDGFRA by 50%. Dasatinib 25-34 factor interacting with PAPOLA and CPSF1 Homo sapiens 141-147 21821988-9 2011 The peak level (Cmax) of dasatinib in this patient was 55.3 nM, which exceeded the concentration of dasatinib required to inhibit cells with FIP1L1-PDGFRA by 50%. Dasatinib 100-109 factor interacting with PAPOLA and CPSF1 Homo sapiens 141-147 21641642-8 2011 Imatinib is effective in patients with increased mast cells and eosinophils associated with FIP1L1/PDGFRA+ (e.g., myeloid neoplasm with eosinophilia and rearrangement of PDGFRA) or rare patients with SM associated with KIT mutations outside of exon 17. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 92-98 21463117-7 2011 Imatinib has been used successfully to treat patients with chronic eosinophilic disorders with the FIP1L1-PDGFRA fusion kinase; limited clinical data indicate that dasatinib could be active in imatinib-resistant disease. Dasatinib 164-173 factor interacting with PAPOLA and CPSF1 Homo sapiens 99-105 21224473-9 2011 In conclusion, our data provide evidence that imatinib-sensitive PDGFRA point mutations play an important role in the pathogenesis of HES and we propose that more research should be performed to further define the frequency and treatment response of PDGFRA mutations in FIP1L1-PDGFRA-negative HES patients. Imatinib Mesylate 46-54 factor interacting with PAPOLA and CPSF1 Homo sapiens 270-276 21327932-0 2011 Durable remission after treatment with very low doses of imatinib for FIP1L1-PDGFRalpha-positive chronic eosinophilic leukaemia. Imatinib Mesylate 57-65 factor interacting with PAPOLA and CPSF1 Homo sapiens 70-76 20565230-5 2010 The tyrosine kinase inhibitor, imatinib, is first-line treatment for FIP1L1-PDGFRA-positive patients). Imatinib Mesylate 31-39 factor interacting with PAPOLA and CPSF1 Homo sapiens 69-75 20832858-0 2011 Low-dose Nilotinib can maintain complete molecular remissions in FIP1L1/PDGFRA-positive hypereosinophilic syndrome. nilotinib 9-18 factor interacting with PAPOLA and CPSF1 Homo sapiens 65-71 20955401-7 2010 One patient had a PDGFRA/FIP1L1 fusion and achieved hematologic and molecular remission after imatinib therapy. Imatinib Mesylate 94-102 factor interacting with PAPOLA and CPSF1 Homo sapiens 25-31 21306153-4 2011 Without the addition of any oxygen-evolving catalysts, we obtained photocurrents of 1.6 and 2.7 mA/cm(2) at 1.23 and 1.53 V vs RHE, respectively. Oxygen 28-34 factor interacting with PAPOLA and CPSF1 Homo sapiens 127-130 21093052-0 2011 Rapid reversal of quadraparesis in chronic eosinophilic leukaemia expressing the FIP1L1-PDGFRA transcript after therapy with imatinib. Imatinib Mesylate 125-133 factor interacting with PAPOLA and CPSF1 Homo sapiens 81-87 21281241-0 2011 Concomitant FIP1L1-PDGFRA fusion gene and T-cell clonality in a case of chronic eosinophilic leukemia with clonal evolution and an incomplete response to imatinib. Imatinib Mesylate 154-162 factor interacting with PAPOLA and CPSF1 Homo sapiens 12-18 20167399-8 2010 CONCLUSION: This report evidences the association of polyserositis with hypereosinophilic syndromes and the potential efficacy of imatinib mesylate even in FIP1L1-PDGFRA-negative patients. Imatinib Mesylate 130-138 factor interacting with PAPOLA and CPSF1 Homo sapiens 156-162 20686211-8 2010 The aim of this study was to develop a new method using the RhE in evaluation of skin irritation caused by alcohol-based hand rubs. Alcohols 107-114 factor interacting with PAPOLA and CPSF1 Homo sapiens 60-63 19728396-1 2010 A small subgroup of patients with hypereosinophilic syndrome (HES) demonstrates imatinib-sensitive fusion transcript-the FIP1L1-PDGFRA (F/P+). Imatinib Mesylate 80-88 factor interacting with PAPOLA and CPSF1 Homo sapiens 121-127 20167399-0 2010 [Efficiency of imatinib in polyserositis revealing a FIP1L1-PDGFRA-negative hypereosinophilic syndrome]. Imatinib Mesylate 15-23 factor interacting with PAPOLA and CPSF1 Homo sapiens 53-59 20167399-2 2010 Imatinib mesylate is the reference treatment for myeloid variants of FIP1L1-PDGFRA-positive hypereosinophilic syndromes. Imatinib Mesylate 0-17 factor interacting with PAPOLA and CPSF1 Homo sapiens 69-75 19910029-8 2009 Imatinib (used in 68 patients) was more effective in patients with the FIP1L1-PDGFRA mutation (88%) than in those without (23%; P < .001). Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 71-77 20167399-3 2010 A response to imatinib has also been reported in FIP1L1-PDGFRA-negative hypereosinophilic syndromes. Imatinib Mesylate 14-22 factor interacting with PAPOLA and CPSF1 Homo sapiens 49-55 19733228-8 2010 The SkinEthic RHE test method showed to be relevant and reliable with a sensitivity of 90% and a specificity of 80% (MTT only) and was not improved by integrating another endpoint such as IL-1alpha. monooxyethylene trimethylolpropane tristearate 117-120 factor interacting with PAPOLA and CPSF1 Homo sapiens 14-17 20726440-3 2010 In addition, we have identified the small molecule inhibitor sorafenib as a potent inhibitor of the FIP1L1-PDGFRA and its T674I imatinib resistant mutant. Sorafenib 61-70 factor interacting with PAPOLA and CPSF1 Homo sapiens 100-106 20726440-4 2010 Sorafenib was originally developed as a BRAF inhibitor, but our work demonstrates that sorafenib can also be used to treat FIP1L1-PDGFRA positive leukemia, demonstrating that new therapies to treat rare leukemias may be simply found by testing drugs that are already in use for the treatment of other diseases. Sorafenib 0-9 factor interacting with PAPOLA and CPSF1 Homo sapiens 123-129 20726440-4 2010 Sorafenib was originally developed as a BRAF inhibitor, but our work demonstrates that sorafenib can also be used to treat FIP1L1-PDGFRA positive leukemia, demonstrating that new therapies to treat rare leukemias may be simply found by testing drugs that are already in use for the treatment of other diseases. Sorafenib 87-96 factor interacting with PAPOLA and CPSF1 Homo sapiens 123-129 20558942-0 2010 Pure red cell aplasia associated with imatinib-treated FIP1L1-PDGFRA positive chronic eosinophilic leukemia. Imatinib Mesylate 38-46 factor interacting with PAPOLA and CPSF1 Homo sapiens 55-61 19735261-3 2009 CR was achieved in 11/23 patients (6/6 with FIP1L1-PDGRFA rearrangement and 5/17 without, P = 0.006), most after 2 weeks of 100 mg/d imatinib. Chromium 0-2 factor interacting with PAPOLA and CPSF1 Homo sapiens 44-50 19735261-5 2009 Low-dose, short-course imatinib may represent a rational choice for identifying responsive cases, both within and outside the pre-defined FIP1L1 rearrangement subset. Imatinib Mesylate 23-31 factor interacting with PAPOLA and CPSF1 Homo sapiens 138-144 19535210-1 2009 The permeation of essential oils through SkinEthic reconstructed human epidermis, (RHE), was studied in vitro to establish a convenient tool to monitor the kinetics of release of active principles from cosmetic formulations. Oils, Volatile 18-32 factor interacting with PAPOLA and CPSF1 Homo sapiens 83-86 19671059-0 2009 Triptolide abrogates oncogene FIP1L1-PDGFRalpha addiction and induces apoptosis in hypereosinophilic syndrome. triptolide 0-10 factor interacting with PAPOLA and CPSF1 Homo sapiens 30-36 19671059-2 2009 HES usually shows good response to the tyrosine kinase inhibitor imatinib, but mutations in FIP1L1-PDGFRalpha (e.g. T674I) can confer acquired resistance to imatinib. Imatinib Mesylate 157-165 factor interacting with PAPOLA and CPSF1 Homo sapiens 92-98 19671059-5 2009 We used low concentrations of triptolide, a transcription inhibitor, to shut down the expression of FIP1L1-PDGFRalpha. triptolide 30-40 factor interacting with PAPOLA and CPSF1 Homo sapiens 100-106 19671059-7 2009 The results revealed that at nanomolar concentrations triptolide decreased the levels of mRNA and protein of FIP1L1-PDGFRalpha and the growth of the neoplastic cells, regardless of the mutational status of PDGFRalpha. triptolide 54-64 factor interacting with PAPOLA and CPSF1 Homo sapiens 109-115 19671059-10 2009 In conclusion, triptolide has potent activity against malignant cells in HES bearing FIP1L1-PDGFRalpha, regardless of its mutational status that confer acquired resistance to imatinib. triptolide 15-25 factor interacting with PAPOLA and CPSF1 Homo sapiens 85-91 19518130-3 2009 These pentacene structures and the reconstructed Au(111) substrate were stable between 0.2 and 0.8 V [vs reversible hydrogen electrode, RHE]. pentacene 6-15 factor interacting with PAPOLA and CPSF1 Homo sapiens 136-139 19518130-3 2009 These pentacene structures and the reconstructed Au(111) substrate were stable between 0.2 and 0.8 V [vs reversible hydrogen electrode, RHE]. Gold 49-51 factor interacting with PAPOLA and CPSF1 Homo sapiens 136-139 19212337-0 2009 FIP1L1-PDGFRalpha D842V, a novel panresistant mutant, emerging after treatment of FIP1L1-PDGFRalpha T674I eosinophilic leukemia with single agent sorafenib. Sorafenib 146-155 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 19144405-0 2009 Success of short-term, higher-dose imatinib mesylate to induce clinical response in FIP1L1-PDGFRalpha-negative hypereosinophilic syndrome. Imatinib Mesylate 35-52 factor interacting with PAPOLA and CPSF1 Homo sapiens 84-90 19144405-1 2009 Presence of the oncogenic mutation FIP1L1-PDGFRalpha in hypereosinophilic patients is predictive of hematologic response to imatinib mesylate. Imatinib Mesylate 124-141 factor interacting with PAPOLA and CPSF1 Homo sapiens 35-41 19144405-3 2009 A patient with FIP1L1-PDGFRalpha-negative HES who had intolerance of interferon alpha-2b and hydroxyurea was treated with escalating doses of imatinib. Hydroxyurea 93-104 factor interacting with PAPOLA and CPSF1 Homo sapiens 15-21 19144405-3 2009 A patient with FIP1L1-PDGFRalpha-negative HES who had intolerance of interferon alpha-2b and hydroxyurea was treated with escalating doses of imatinib. Imatinib Mesylate 142-150 factor interacting with PAPOLA and CPSF1 Homo sapiens 15-21 19951530-9 2009 CONCLUSION: Imatinib in treatment of MPN with eosinophilia and positive FIP1L1-PDGFR alpha gene patients can induce high hematologic and molecular remission. Imatinib Mesylate 12-20 factor interacting with PAPOLA and CPSF1 Homo sapiens 72-78 19246139-8 2009 In a group of patients, oncogenic tyrosine kinases (TK) such as FIP1L1/PDGFRA, can be employed as therapeutic targets by using imatinib or other TK-blocking agents. Imatinib Mesylate 127-135 factor interacting with PAPOLA and CPSF1 Homo sapiens 64-70 19210352-1 2009 BACKGROUND: The Fip1-like-1-platelet-derived growth factor receptor alpha (FIP1L1-PDGFRA) gene fusion is a common cause of chronic eosinophilic leukemia (CEL)/hypereosinophilic syndrome (HES), and patients suffering from this particular subgroup of CEL/HES respond to low-dose imatinib therapy. Imatinib Mesylate 277-285 factor interacting with PAPOLA and CPSF1 Homo sapiens 75-81 19210352-3 2009 METHODS: In an imatinib resistant FIP1L1-PDGFRA positive patient, we analyzed the molecular structure of the fusion gene and analyzed the effect of several kinase inhibitors on FIP1L1-PDGFRA-mediated proliferative responses in vitro. Imatinib Mesylate 15-23 factor interacting with PAPOLA and CPSF1 Homo sapiens 34-40 19210352-3 2009 METHODS: In an imatinib resistant FIP1L1-PDGFRA positive patient, we analyzed the molecular structure of the fusion gene and analyzed the effect of several kinase inhibitors on FIP1L1-PDGFRA-mediated proliferative responses in vitro. Imatinib Mesylate 15-23 factor interacting with PAPOLA and CPSF1 Homo sapiens 177-183 19210352-6 2009 Moreover, sorafenib, which has been described to inhibit T674I mutant FIP1L1-PDGFRA, failed to block S601P mutant FIP1L1-PDGFRA. Sorafenib 10-19 factor interacting with PAPOLA and CPSF1 Homo sapiens 70-76 19210352-8 2009 CONCLUSIONS: We identified a novel mutation in FIP1L1-PDGFRA resulting in both imatinib and sorafenib resistance. Imatinib Mesylate 79-87 factor interacting with PAPOLA and CPSF1 Homo sapiens 47-53 19210352-8 2009 CONCLUSIONS: We identified a novel mutation in FIP1L1-PDGFRA resulting in both imatinib and sorafenib resistance. Sorafenib 92-101 factor interacting with PAPOLA and CPSF1 Homo sapiens 47-53 19212337-2 2009 Most FIP1L1-PDGFRA positive patients enjoy durable and complete molecular responses to low-dose imatinib (Glivec/Gleevec). Imatinib Mesylate 96-104 factor interacting with PAPOLA and CPSF1 Homo sapiens 5-11 19212337-4 2009 We describe a case of FIP1L1-PDGFRalpha T674I CEL in blast crisis that responded to sorafenib (Nexavar). Sorafenib 84-93 factor interacting with PAPOLA and CPSF1 Homo sapiens 22-28 19212337-4 2009 We describe a case of FIP1L1-PDGFRalpha T674I CEL in blast crisis that responded to sorafenib (Nexavar). Sorafenib 95-102 factor interacting with PAPOLA and CPSF1 Homo sapiens 22-28 19212337-7 2009 In vitro, the novel FIP1L1-PDGFRalpha D842V mutant is highly resistant to sorafenib, imatinib, dasatinib (Sprycell) and PKC412 (Midostaurin). Sorafenib 74-83 factor interacting with PAPOLA and CPSF1 Homo sapiens 20-26 19212337-7 2009 In vitro, the novel FIP1L1-PDGFRalpha D842V mutant is highly resistant to sorafenib, imatinib, dasatinib (Sprycell) and PKC412 (Midostaurin). Imatinib Mesylate 85-93 factor interacting with PAPOLA and CPSF1 Homo sapiens 20-26 19212337-7 2009 In vitro, the novel FIP1L1-PDGFRalpha D842V mutant is highly resistant to sorafenib, imatinib, dasatinib (Sprycell) and PKC412 (Midostaurin). Dasatinib 95-104 factor interacting with PAPOLA and CPSF1 Homo sapiens 20-26 19212337-7 2009 In vitro, the novel FIP1L1-PDGFRalpha D842V mutant is highly resistant to sorafenib, imatinib, dasatinib (Sprycell) and PKC412 (Midostaurin). midostaurin 128-139 factor interacting with PAPOLA and CPSF1 Homo sapiens 20-26 19212337-8 2009 Thus, sorafenib is clinically active in imatinib-resistant FIP1L1-PDGFRalpha T674I CEL, but the rapid emergence of other mutants may limit the response duration. Sorafenib 6-15 factor interacting with PAPOLA and CPSF1 Homo sapiens 59-65 19212337-8 2009 Thus, sorafenib is clinically active in imatinib-resistant FIP1L1-PDGFRalpha T674I CEL, but the rapid emergence of other mutants may limit the response duration. Imatinib Mesylate 40-48 factor interacting with PAPOLA and CPSF1 Homo sapiens 59-65 19224921-5 2009 Furthermore, tert-butylhydroquinone (tBHQ), an agent that induces oxidative stress, increased the phosphorylation level of IRBIT in vivo and in parallel enhanced the interaction between IRBIT and CPSF and promoted the cytoplasmic distribution of endogenous Fip1. 2-tert-butylhydroquinone 13-35 factor interacting with PAPOLA and CPSF1 Homo sapiens 257-261 19224921-5 2009 Furthermore, tert-butylhydroquinone (tBHQ), an agent that induces oxidative stress, increased the phosphorylation level of IRBIT in vivo and in parallel enhanced the interaction between IRBIT and CPSF and promoted the cytoplasmic distribution of endogenous Fip1. 2-tert-butylhydroquinone 37-41 factor interacting with PAPOLA and CPSF1 Homo sapiens 257-261 19187542-1 2009 BACKGROUND: Primary eosinophlia associated with the FIP1L1-PDGFRA rearrangement represents a subset of chronic eosinophilic leukaemia (CEL) and affected patients are very sensitive to imatinib treatment. Imatinib Mesylate 184-192 factor interacting with PAPOLA and CPSF1 Homo sapiens 52-58 19224921-4 2009 The main target for IRBIT in CPSF was Fip1 subunit, and the phosphorylation of the serine-rich region of IRBIT was required both for direct association with Fip1 in vitro and for redistribution of Fip1 into the cytoplasm of intact cells. Serine 83-89 factor interacting with PAPOLA and CPSF1 Homo sapiens 157-161 19224921-4 2009 The main target for IRBIT in CPSF was Fip1 subunit, and the phosphorylation of the serine-rich region of IRBIT was required both for direct association with Fip1 in vitro and for redistribution of Fip1 into the cytoplasm of intact cells. Serine 83-89 factor interacting with PAPOLA and CPSF1 Homo sapiens 157-161 19120352-0 2009 Weekly imatinib dosage for chronic eosinophilic leukaemia expressing FIP1L1-PDGFRA fusion transcript: extended follow-up. Imatinib Mesylate 7-15 factor interacting with PAPOLA and CPSF1 Homo sapiens 69-75 19271173-6 2009 CONCLUSIONS: YXS capsule combined with RHE shows a better therapeutic effect in treating NA than that of RHE alone, and the effect might be through stimulation by YXS of erythropoiesis which could promote the secretion of testosterone. Testosterone 222-234 factor interacting with PAPOLA and CPSF1 Homo sapiens 39-42 19080234-16 2008 CONCLUSION: The present case fulfilled the WHO diagnostic criteria of FIP1L1/PDGFRalpha(-) CEL which did not respond to routine treatment and imatinib. Imatinib Mesylate 142-150 factor interacting with PAPOLA and CPSF1 Homo sapiens 70-76 18843283-3 2008 A few prospective trials have now better defined the natural history of imatinib-treated FIP1L1-PDGFRA-positive patients, from which some basic conclusions can be drawn: the prognosis is outstanding, acquired resistance is exceedingly rare, but ongoing imatinib treatment is likely required to prevent relapse. Imatinib Mesylate 72-80 factor interacting with PAPOLA and CPSF1 Homo sapiens 89-95 19096755-3 2009 Despite patients with FIP1-like-1-platelet-derived growth factor alpha (FIP1L1-PDGFRA) associated HES (myeloid neoplasms associated with PDGFRA rearrangement) have been shown to respond to low-dose imatinib with a complete and durable hematological and cytogenetic remission, influences of imatinib on clinical manifestations related to hypereosinophilia heart involvement are variable. Imatinib Mesylate 198-206 factor interacting with PAPOLA and CPSF1 Homo sapiens 72-78 19096755-3 2009 Despite patients with FIP1-like-1-platelet-derived growth factor alpha (FIP1L1-PDGFRA) associated HES (myeloid neoplasms associated with PDGFRA rearrangement) have been shown to respond to low-dose imatinib with a complete and durable hematological and cytogenetic remission, influences of imatinib on clinical manifestations related to hypereosinophilia heart involvement are variable. Imatinib Mesylate 290-298 factor interacting with PAPOLA and CPSF1 Homo sapiens 72-78 18307562-0 2008 A single weekly dose of imatinib is sufficient to induce and maintain remission of chronic eosinophilic leukaemia in FIP1L1-PDGFRA-expressing patients. Imatinib Mesylate 24-32 factor interacting with PAPOLA and CPSF1 Homo sapiens 117-123 18619723-0 2008 Dasatinib inhibits the growth and survival of neoplastic human eosinophils (EOL-1) through targeting of FIP1L1-PDGFRalpha. Dasatinib 0-9 factor interacting with PAPOLA and CPSF1 Homo sapiens 104-110 18619723-4 2008 The tyrosine kinase (TK) inhibitor imatinib (STI571) has been described to counteract the TK activity of FIP1L1-PDGFRalpha in most patients. Imatinib Mesylate 35-43 factor interacting with PAPOLA and CPSF1 Homo sapiens 105-111 18619723-4 2008 The tyrosine kinase (TK) inhibitor imatinib (STI571) has been described to counteract the TK activity of FIP1L1-PDGFRalpha in most patients. Imatinib Mesylate 45-51 factor interacting with PAPOLA and CPSF1 Homo sapiens 105-111 18619723-7 2008 MATERIALS AND METHODS: We provide evidence that dasatinib, a multi-targeted kinase inhibitor, blocks the growth and survival of EOL-1, an eosinophil leukemia cell line carrying FIP1L1-PDGFRalpha. Dasatinib 48-57 factor interacting with PAPOLA and CPSF1 Homo sapiens 177-183 18619723-11 2008 In Western blot experiments, dasatinib completely blocked the phosphorylation of FIP1L1-PDGFRalpha in EOL-1 cells. Dasatinib 29-38 factor interacting with PAPOLA and CPSF1 Homo sapiens 81-87 18619723-12 2008 CONCLUSIONS: Dasatinib inhibits the growth of leukemic eosinophils through targeting of the disease-related oncoprotein FIP1L1-PDGFRalpha. Dasatinib 13-22 factor interacting with PAPOLA and CPSF1 Homo sapiens 120-126 18706197-0 2008 FIP1L1-PDGFRalpha alone or with other genetic abnormalities reveals disease progression in chronic eosinophilic leukemia but good response to imatinib. Imatinib Mesylate 142-150 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 18706197-1 2008 BACKGROUND: The FIP1L1-PDGFRalpha fusion gene plays an important role in the pathogenesis of chronic eosinophilic leukemia (CEL) and is a direct therapeutic target of the tyrosine kinase inhibitor imatinib mesylate. Imatinib Mesylate 197-214 factor interacting with PAPOLA and CPSF1 Homo sapiens 16-22 18706197-6 2008 Nevertheless, imatinib mesylate induced rapid and complete hematological responses in treated FIP1L1-PDGFRalpha cases, followed by molecular remission and reversal of myelofibrosis. Imatinib Mesylate 14-31 factor interacting with PAPOLA and CPSF1 Homo sapiens 94-100 18309036-2 2008 Ki11502 (0.1-1 nM, 2 days) profoundly caused growth arrest, G(0)/G(1) cell-cycle arrest, and apoptosis associated with down-regulation of Bcl-2 family proteins in the eosinophilic leukemia EOL-1 cells having the activated FIP1-like 1/PDGFRalpha fusion gene. Ki11502 0-7 factor interacting with PAPOLA and CPSF1 Homo sapiens 222-233 18826333-6 2008 The permeation rates of the steroids were ranked as: alveolar model >> RHE > FT-model, pig skin > human skin. Steroids 28-36 factor interacting with PAPOLA and CPSF1 Homo sapiens 77-80 18549340-6 2008 RESULTS/CONCLUSION: The development of imatinib-resistant mutations in the FIP1L1-PDGFR-alpha kinase domain has spurred the development of an array of new tyrosine kinase inhibitors. Imatinib Mesylate 39-47 factor interacting with PAPOLA and CPSF1 Homo sapiens 75-81 18307562-2 2008 A subset of HES patients presents an interstitial deletion in chromosome 4q12, which leads to the expression of an imatinib-responsive fusion gene, FIP1L1-PDGFRA. Imatinib Mesylate 115-123 factor interacting with PAPOLA and CPSF1 Homo sapiens 148-154 18307562-10 2008 These data suggest that a single weekly dose of imatinib is sufficient to maintain remission in FIP1L1-PDGFRA- positive CEL patients. Imatinib Mesylate 48-56 factor interacting with PAPOLA and CPSF1 Homo sapiens 96-102 18214408-6 2008 Patients with hypereosinophilic syndrome should be tested for the presence of the FIP1L1-PDGRFA-mutatition in order to identify patients that could benefit from a treatment with a tyrosine kinase inhibitor such as Imatinib. Imatinib Mesylate 214-222 factor interacting with PAPOLA and CPSF1 Homo sapiens 82-88 17915318-1 2008 Imatinib and retinoids induce apoptosis in FIP1L1/PDGFRalpha-positive EoL-1 leukemia cells. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 43-49 18194138-9 2008 Recently, the resulting FIP1L1-PDGFRalpha fusion gene was characterized as a marker of response to imatinib. Imatinib Mesylate 99-107 factor interacting with PAPOLA and CPSF1 Homo sapiens 24-30 18086564-4 2008 The FIP1L1-PDGFRalpha inhibitor imatinib inhibited the proliferation of EoL-1 cells and decreased the level of the oncoprotein c-Myc as well as the phosphorylation of extracellular signal-regulated kinase and c-Jun N-terminal kinase (JNK). Imatinib Mesylate 32-40 factor interacting with PAPOLA and CPSF1 Homo sapiens 4-10 17915318-1 2008 Imatinib and retinoids induce apoptosis in FIP1L1/PDGFRalpha-positive EoL-1 leukemia cells. Retinoids 13-22 factor interacting with PAPOLA and CPSF1 Homo sapiens 43-49 17915318-2 2008 Although imatinib induces complete remission in most FIP1L1/PDGFRalpha-positive patients, response to imatinib is sometimes suboptimal. Imatinib Mesylate 9-17 factor interacting with PAPOLA and CPSF1 Homo sapiens 53-59 18504399-3 2008 The HDAC inhibitors apicidin and n-butyrate suppress the proliferation of EoL-1 cells and induce differentiation into eosinophils by a decrease in the protein level of FIP1L1-PDGFRalpha without affecting the mRNA level for FIP1L1-PDGFRA. apicidin 20-28 factor interacting with PAPOLA and CPSF1 Homo sapiens 168-174 18504399-3 2008 The HDAC inhibitors apicidin and n-butyrate suppress the proliferation of EoL-1 cells and induce differentiation into eosinophils by a decrease in the protein level of FIP1L1-PDGFRalpha without affecting the mRNA level for FIP1L1-PDGFRA. apicidin 20-28 factor interacting with PAPOLA and CPSF1 Homo sapiens 223-229 18504399-3 2008 The HDAC inhibitors apicidin and n-butyrate suppress the proliferation of EoL-1 cells and induce differentiation into eosinophils by a decrease in the protein level of FIP1L1-PDGFRalpha without affecting the mRNA level for FIP1L1-PDGFRA. Butyrates 33-43 factor interacting with PAPOLA and CPSF1 Homo sapiens 168-174 18504399-3 2008 The HDAC inhibitors apicidin and n-butyrate suppress the proliferation of EoL-1 cells and induce differentiation into eosinophils by a decrease in the protein level of FIP1L1-PDGFRalpha without affecting the mRNA level for FIP1L1-PDGFRA. Butyrates 33-43 factor interacting with PAPOLA and CPSF1 Homo sapiens 223-229 18504399-4 2008 In this study, we analyzed the mechanism by which the protein level of FIP1L1-PDGFRalpha is decreased by apicidin and n-butyrate. apicidin 105-113 factor interacting with PAPOLA and CPSF1 Homo sapiens 71-77 18504399-4 2008 In this study, we analyzed the mechanism by which the protein level of FIP1L1-PDGFRalpha is decreased by apicidin and n-butyrate. Butyrates 118-128 factor interacting with PAPOLA and CPSF1 Homo sapiens 71-77 18504399-7 2008 Actinomycin D and cycloheximide were used to block RNA synthesis and protein synthesis, respectively, in the chasing experiment of the amount of FIP1L1-PDGFRalpha protein. Dactinomycin 0-13 factor interacting with PAPOLA and CPSF1 Homo sapiens 145-151 18504399-7 2008 Actinomycin D and cycloheximide were used to block RNA synthesis and protein synthesis, respectively, in the chasing experiment of the amount of FIP1L1-PDGFRalpha protein. Cycloheximide 18-31 factor interacting with PAPOLA and CPSF1 Homo sapiens 145-151 18504399-8 2008 RESULTS: When apicidin- and n-butyrate-treated EoL-1 cells were incubated in the presence of actinomycin D, the decrease in the protein level of FIP1L1-PDGFRalpha was significantly enhanced when compared with controls. apicidin 14-22 factor interacting with PAPOLA and CPSF1 Homo sapiens 145-151 18504399-8 2008 RESULTS: When apicidin- and n-butyrate-treated EoL-1 cells were incubated in the presence of actinomycin D, the decrease in the protein level of FIP1L1-PDGFRalpha was significantly enhanced when compared with controls. Butyrates 28-38 factor interacting with PAPOLA and CPSF1 Homo sapiens 145-151 18504399-8 2008 RESULTS: When apicidin- and n-butyrate-treated EoL-1 cells were incubated in the presence of actinomycin D, the decrease in the protein level of FIP1L1-PDGFRalpha was significantly enhanced when compared with controls. Dactinomycin 93-106 factor interacting with PAPOLA and CPSF1 Homo sapiens 145-151 17544504-1 2008 Patients with primary hypereosinophilic disorders who are positive for the FIP1L1-PDGFRA fusion gene mutation are highly responsive to therapy with imatinib mesylate. Imatinib Mesylate 148-165 factor interacting with PAPOLA and CPSF1 Homo sapiens 75-81 17544504-2 2008 A 35-year-old man with FIP1L1-PDGFRA positive hypereosinophilic syndrome and cardiac involvement, was treated with imatinib 100 mg daily. Imatinib Mesylate 115-123 factor interacting with PAPOLA and CPSF1 Homo sapiens 23-29 17709602-0 2007 Relapse following discontinuation of imatinib mesylate therapy for FIP1L1/PDGFRA-positive chronic eosinophilic leukemia: implications for optimal dosing. Imatinib Mesylate 37-54 factor interacting with PAPOLA and CPSF1 Homo sapiens 67-73 18036706-0 2008 [Efficacy of imatinib in FIP1L1-PDGFRA positive hypereosinophilic syndrome]. Imatinib Mesylate 13-21 factor interacting with PAPOLA and CPSF1 Homo sapiens 25-31 18203417-0 2007 [Identification of clonal proliferation of T cell and FIP1L1-PDGFRalpha fusion gene in hypereosinophilic syndrome associated with lymphomatoid papulosis which showed rapid and complete response to the treatment with imatinib]. Imatinib Mesylate 216-224 factor interacting with PAPOLA and CPSF1 Homo sapiens 54-60 17709602-1 2007 Although imatinib is clearly the treatment of choice for FIP1L1/PDGFRA-positive chronic eosinophilic leukemia (CEL), little is known about optimal dosing, duration of treatment, and the possibility of cure in this disorder. Imatinib Mesylate 9-17 factor interacting with PAPOLA and CPSF1 Homo sapiens 57-63 18004179-13 2007 We consider the coadministration of corticosteroids and hydroxyurea to be an effective combination for the treatment of FIP1L1-PDGFRA-negative HES. Hydroxyurea 56-67 factor interacting with PAPOLA and CPSF1 Homo sapiens 120-126 17488167-10 2007 In contrast, patients carrying the FIP1L1-PDGFRA mutation achieve complete responses with low-dose imatinib therapy. Imatinib Mesylate 99-107 factor interacting with PAPOLA and CPSF1 Homo sapiens 35-41 17988989-0 2007 Successful imatinib treatment of cardiac involvement of FIP1L1-PDGFRA-positive chronic eosinophilic leukemia followed by severe hepatotoxicity. Imatinib Mesylate 11-19 factor interacting with PAPOLA and CPSF1 Homo sapiens 56-62 17988989-1 2007 Imatinib is highly effective for the treatment of chronic eosinophilic leukemia (CEL) caused by the FIP1L1-PDGFRA fusion gene. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 100-106 17988989-13 2007 Thus, imatinib may be very effective for treating the early cardiac involvement of FIP1L1-PDGFRA-positive CEL, but it needs to be used cautiously. Imatinib Mesylate 6-14 factor interacting with PAPOLA and CPSF1 Homo sapiens 83-89 17940488-4 2007 Karyotypically occult FIP1L1- platelet-derived growth factor receptor alpha and beta rearranged eosinophilic disorders respond to imatinib mesylate with almost 100% efficacy. Imatinib Mesylate 130-147 factor interacting with PAPOLA and CPSF1 Homo sapiens 22-28 17940488-5 2007 If standard therapies fail, the FIP1L1- platelet-derived growth factor receptor-negative cases of hypereosinophilic syndrome should also be considered for treatment with imatinib. Imatinib Mesylate 170-178 factor interacting with PAPOLA and CPSF1 Homo sapiens 32-38 17940488-10 2007 The FIP1L1- platelet-derived growth factor receptor alpha-negative responders to imatinib pose a question as to the existence of subentities with unrecognized tyrosine kinases-based mutation. Imatinib Mesylate 81-89 factor interacting with PAPOLA and CPSF1 Homo sapiens 4-10 17666373-0 2007 The efficacy of imatinib mesylate in patients with FIP1L1-PDGFRalpha-positive hypereosinophilic syndrome. Imatinib Mesylate 16-33 factor interacting with PAPOLA and CPSF1 Homo sapiens 51-57 17666373-3 2007 These cases with FIP1L1-PDGFRalpha rearrangement have been reported to be very sensitive to the tyrosine kinase inhibitor imatinib mesylate. Imatinib Mesylate 122-139 factor interacting with PAPOLA and CPSF1 Homo sapiens 17-23 17593250-0 2007 Charcot-Leyden crystals in the trephine biopsy of a patient with a FIP1L1-PDGFRA - positive myeloproliferative disorder. trephine 31-39 factor interacting with PAPOLA and CPSF1 Homo sapiens 67-73 17495975-0 2007 The novel tyrosine kinase inhibitor EXEL-0862 induces apoptosis in human FIP1L1-PDGFR-alpha-expressing cells through caspase-3-mediated cleavage of Mcl-1. exel-0862 36-45 factor interacting with PAPOLA and CPSF1 Homo sapiens 73-79 17495975-5 2007 EXEL-0862 inhibited the proliferation of EOL-1 and imatinib-resistant T674I FIP1L1-PDGFR-alpha-expressing cells and resulted in potent inhibition of the phosphorylation of PDGFR-alpha and downstream proteins STAT3 and Erk1/2, both in vitro and ex vivo. Imatinib Mesylate 51-59 factor interacting with PAPOLA and CPSF1 Homo sapiens 76-82 17299092-0 2007 Low-dose imatinib mesylate leads to rapid induction of major molecular responses and achievement of complete molecular remission in FIP1L1-PDGFRA-positive chronic eosinophilic leukemia. Imatinib Mesylate 9-26 factor interacting with PAPOLA and CPSF1 Homo sapiens 132-138 17299092-1 2007 The FIP1L1-PDGFRA fusion gene is a recurrent molecular lesion in eosinophilia-associated myeloproliferative disorders, predicting a favorable response to imatinib mesylate. Imatinib Mesylate 154-171 factor interacting with PAPOLA and CPSF1 Homo sapiens 4-10 17299092-5 2007 Normalized FIP1L1-PDGFRA transcript levels in patient samples prior to imatinib varied by almost 3 logs. Imatinib Mesylate 71-79 factor interacting with PAPOLA and CPSF1 Homo sapiens 11-17 17299092-8 2007 In 2 patients, withdrawal of imatinib was followed by a rapid rise in FIP1L1-PDGFRA transcript levels. Imatinib Mesylate 29-37 factor interacting with PAPOLA and CPSF1 Homo sapiens 70-76 17299092-9 2007 Overall, these data are consistent with the exquisite sensitivity of the FIP1L1-PDGFRalpha fusion to imatinib, as compared with BCR-ABL, and underline the importance of RQ-PCR monitoring to guide management using molecularly targeted therapies. Imatinib Mesylate 101-109 factor interacting with PAPOLA and CPSF1 Homo sapiens 73-79 17495975-6 2007 Moreover, EXEL-0862 induced apoptotic death in EOL-1 cells and imatinib-resistant T674I FIP1L1-PDGFR-alpha-expressing cells, and resulted in significant downregulation of the antiapoptotic protein Mcl-1 through a caspase-dependent mechanism. Imatinib Mesylate 63-71 factor interacting with PAPOLA and CPSF1 Homo sapiens 88-94 17440089-1 2007 An interstitial deletion on chromosome 4q12 resulting in the formation of the FIP1L1-PDGFRA fusion protein is involved in the pathogenesis of imatinib-sensitive chronic eosinophilic leukemia. Imatinib Mesylate 142-150 factor interacting with PAPOLA and CPSF1 Homo sapiens 78-84 17440089-4 2007 FIP1L1-PDGFRA induced both proliferation and differentiation of eosinophils, neutrophils, and erythrocytes in the absence of cytokines, which could be inhibited by imatinib. Imatinib Mesylate 164-172 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 17541270-2 2007 Recent studies examining eosinophil biology have focused on delineating the molecular basis of FIP1L1/PDGRFalpha-fusion gene induced HES, the molecular steps involved in eosinophil recruitment in tumor-associated eosinophilia and EGID, and the role of eosinophils in asthma. Helium 133-136 factor interacting with PAPOLA and CPSF1 Homo sapiens 95-101 17258775-4 2007 It was demonstrated that apicidin and n-butyrate induced a continuous acetylation of histones H4 and H3, inhibited the proliferation of EoL-1 cells without attenuating the level of FIP1L1-PDGFRA mRNA, and induced the expression of markers for mature eosinophils such as integrin beta7, CCR1, and CCR3 on EoL-1 cells, while trichostatin A evoked a transient acetylation of histones and induced no differentiation into eosinophils. Butyrates 38-48 factor interacting with PAPOLA and CPSF1 Homo sapiens 181-187 17215855-8 2007 This study provided evidence for marked differences in the leukemic masses which are targeted by imatinib in CEL or CML, as harboring FIP1L1-PDGFRA or BCR-ABL1. Imatinib Mesylate 97-105 factor interacting with PAPOLA and CPSF1 Homo sapiens 134-140 17541273-7 2007 RESULTS: Treatment of EoL-1 cells with apicidin at 100 nM or n-butyrate at 500 microM decreased the levels of FIP1L1-PDGFRalpha protein and phosphorylated-Stat5, while that with trichostatin A at 30 nM did not. apicidin 39-47 factor interacting with PAPOLA and CPSF1 Homo sapiens 110-116 17541273-7 2007 RESULTS: Treatment of EoL-1 cells with apicidin at 100 nM or n-butyrate at 500 microM decreased the levels of FIP1L1-PDGFRalpha protein and phosphorylated-Stat5, while that with trichostatin A at 30 nM did not. Butyrates 61-71 factor interacting with PAPOLA and CPSF1 Homo sapiens 110-116 17541273-8 2007 CONCLUSIONS: The decrease in the level of FIP1L1-PDGFRalpha protein caused by apicidin and n-butyrate might be one of the mechanisms by which EoL-1 cells are induced to differentiate into eosinophils by these HDAC inhibitors. apicidin 78-86 factor interacting with PAPOLA and CPSF1 Homo sapiens 42-48 17541273-8 2007 CONCLUSIONS: The decrease in the level of FIP1L1-PDGFRalpha protein caused by apicidin and n-butyrate might be one of the mechanisms by which EoL-1 cells are induced to differentiate into eosinophils by these HDAC inhibitors. Butyrates 91-101 factor interacting with PAPOLA and CPSF1 Homo sapiens 42-48 16965435-1 2006 Fip1-like 1/platelet-derived growth factor receptor-alpha (FIP1L1/PDGFRA)-positive hypereosinophilic syndrome is a rare disorder with a poor prognosis if untreated and for which treatment with imatinib mesilate is highly effective. Imatinib Mesylate 193-210 factor interacting with PAPOLA and CPSF1 Homo sapiens 59-65 16682077-3 2006 Cumulative evidence indicates that the Bcr-Abl tyrosine kinase inhibitor imatinib mesylate (Gleevec) is active for the treatment of patients with HES, particularly those expressing the FIP1L1-PDGFR-alpha oncoprotein. Imatinib Mesylate 73-90 factor interacting with PAPOLA and CPSF1 Homo sapiens 185-191 16682077-3 2006 Cumulative evidence indicates that the Bcr-Abl tyrosine kinase inhibitor imatinib mesylate (Gleevec) is active for the treatment of patients with HES, particularly those expressing the FIP1L1-PDGFR-alpha oncoprotein. Imatinib Mesylate 92-99 factor interacting with PAPOLA and CPSF1 Homo sapiens 185-191 23662039-3 2006 FIP1L1/PDGFRalpha, the product of the gene FIP1L1/PDGFRA, is a constitutively activated tyrosine kinase and can be inhibited by imatinib mesylate. Imatinib Mesylate 128-145 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 23662039-3 2006 FIP1L1/PDGFRalpha, the product of the gene FIP1L1/PDGFRA, is a constitutively activated tyrosine kinase and can be inhibited by imatinib mesylate. Imatinib Mesylate 128-145 factor interacting with PAPOLA and CPSF1 Homo sapiens 43-49 16645167-0 2006 Sorafenib is a potent inhibitor of FIP1L1-PDGFRalpha and the imatinib-resistant FIP1L1-PDGFRalpha T674I mutant. Sorafenib 0-9 factor interacting with PAPOLA and CPSF1 Homo sapiens 35-41 16406018-10 2006 Because of the availability of a superior targeted drug (imatinib), it is of importance to screen for FIP1L1/PDGFRalpha in suspected CEL with or without co-existing SM. Imatinib Mesylate 57-65 factor interacting with PAPOLA and CPSF1 Homo sapiens 102-108 16645167-0 2006 Sorafenib is a potent inhibitor of FIP1L1-PDGFRalpha and the imatinib-resistant FIP1L1-PDGFRalpha T674I mutant. Sorafenib 0-9 factor interacting with PAPOLA and CPSF1 Homo sapiens 80-86 16645167-0 2006 Sorafenib is a potent inhibitor of FIP1L1-PDGFRalpha and the imatinib-resistant FIP1L1-PDGFRalpha T674I mutant. Imatinib Mesylate 61-69 factor interacting with PAPOLA and CPSF1 Homo sapiens 80-86 16645167-1 2006 The FIP1L1-PDGFRA oncogene is a common cause of chronic eosinophilic leukemia (CEL), and encodes an activated tyrosine kinase that is inhibited by imatinib. Imatinib Mesylate 147-155 factor interacting with PAPOLA and CPSF1 Homo sapiens 4-10 16645167-2 2006 FIP1L1-PDGFRA-positive patients with CEL respond to low-dose imatinib therapy, but resistance due to acquired T674I mutation has been observed. Imatinib Mesylate 61-69 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 16645167-3 2006 We report here the identification of sorafenib as a potent inhibitor of the FIP1 like 1-platelet-derived growth factor receptor alpha (FIP1L1-PDGFRalpha) (T674I) mutant. Sorafenib 37-46 factor interacting with PAPOLA and CPSF1 Homo sapiens 135-141 16645167-7 2006 Our data suggest that low doses of sorafenib could be efficient for the treatment of FIP1L1-PDGFRA-positive CEL and could be used to overcome resistance to imatinib associated with the T674I mutation. Sorafenib 35-44 factor interacting with PAPOLA and CPSF1 Homo sapiens 85-91 16690743-5 2006 Instead, truncation of PDGFRalpha between two conserved tryptophan residues in the juxtamembrane (JM) domain is required for kinase activation and transforming potential of FIP1L1-PDGFRalpha. Tryptophan 56-66 factor interacting with PAPOLA and CPSF1 Homo sapiens 173-179 16406016-0 2006 FIP1L1-PDGFRA in eosinophilic disorders: prevalence in routine clinical practice, long-term experience with imatinib therapy, and a critical review of the literature. Imatinib Mesylate 108-116 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 16406016-2 2006 In that series, all 11 FIP1L1-PDGFRA+ patients receiving imatinib achieved a complete response. Imatinib Mesylate 57-65 factor interacting with PAPOLA and CPSF1 Homo sapiens 23-29 16754777-0 2006 The FIP1L1-PDGFRA T674I mutation can be inhibited by the tyrosine kinase inhibitor AMN107 (nilotinib). nilotinib 83-89 factor interacting with PAPOLA and CPSF1 Homo sapiens 4-10 16754777-0 2006 The FIP1L1-PDGFRA T674I mutation can be inhibited by the tyrosine kinase inhibitor AMN107 (nilotinib). nilotinib 91-100 factor interacting with PAPOLA and CPSF1 Homo sapiens 4-10 16612767-4 2006 Indeed, imatinib mesylate has become first-line therapy for patients in whom the FIP1L1-PDGFRalpha fusion gene is detected, whereas corticosteroids remain the mainstay for management of patients in whom hypereosinophilia is secondary to the overproduction of interleukin 5 by abnormal T-cells. Imatinib Mesylate 8-25 factor interacting with PAPOLA and CPSF1 Homo sapiens 81-87 16485879-4 2006 Imatinib has been reported to be an effective treatment for FIP1L1-PDGFRalpha+ mast cell disease, hypereosinophilic syndrome, and dermatofibrosarcoma protuberans. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 60-66 16344672-1 2005 Idiopathic hypereosinophilic syndrome (HES) in children is a very rare disorder; certain clinical differences with adult HES have been described, with no pediatric case with the imatinib-responsive FIP1L1-PDGFRA fusion gene reported to date. Imatinib Mesylate 178-186 factor interacting with PAPOLA and CPSF1 Homo sapiens 198-204 16781490-8 2006 Imatinib mesylate therapy might result in complete remission of SM cases with wild-type KIT, certain KIT mutations, such as F522C, or the FIP1L1-PDGFRA fusion gene, but not of D816V-KIT-bearing SM. Imatinib Mesylate 0-17 factor interacting with PAPOLA and CPSF1 Homo sapiens 138-144 16030188-0 2005 The small molecule tyrosine kinase inhibitor AMN107 inhibits TEL-PDGFRbeta and FIP1L1-PDGFRalpha in vitro and in vivo. nilotinib 45-51 factor interacting with PAPOLA and CPSF1 Homo sapiens 79-85 16479834-0 2005 [Oncogene Fip1-likeL/PDGFRalpha as a target for imatinib in patients with hypereosinophilic syndrome and chronic eosinophilic leukemia. Imatinib Mesylate 48-56 factor interacting with PAPOLA and CPSF1 Homo sapiens 10-14 20477604-5 2005 A subgroup of patients with the myeloproliferative variant carry the new gene rearrangement FIP1L1-PDGFRA, which produces a constitutively active tyrosine kinase often responsive to antityrosine kinase therapy with imatinib mesylate. Imatinib Mesylate 215-232 factor interacting with PAPOLA and CPSF1 Homo sapiens 92-98 15937220-5 2005 CFI(m) is sufficient to direct sequence-specific, A(A/U)UAAA-independent poly(A) addition in vitro through the recruitment of the CPSF subunit hFip1 and poly(A) polymerase to the RNA substrate. Poly A 73-80 factor interacting with PAPOLA and CPSF1 Homo sapiens 143-148 15921304-6 2005 On the basis of FIP1L1-PDGFRa fusion gene hypereosinophilic syndrome would be classified as a clonal disease and in the FIP1L1-PDGFRa positive cases the tyrosine kinase inhibitor imatinib mesylate (Glivec) would be effective. Imatinib Mesylate 179-196 factor interacting with PAPOLA and CPSF1 Homo sapiens 120-126 15618966-0 2005 Myeloid blast crisis evolving during imatinib treatment of an FIP1L1-PDGFR alpha-positive chronic myeloproliferative disease with prominent eosinophilia. Imatinib Mesylate 37-45 factor interacting with PAPOLA and CPSF1 Homo sapiens 62-68 15854548-4 2005 One FIP1L1-PDGFRA fusion gene positive patient was administered with low-dose imatinib. Imatinib Mesylate 78-86 factor interacting with PAPOLA and CPSF1 Homo sapiens 4-10 15854548-7 2005 Continuous hematological remission was observed in one FIP1L1-PDGFRA fusion gene positive HES patient after low-dose imatinib treatment. Imatinib Mesylate 117-125 factor interacting with PAPOLA and CPSF1 Homo sapiens 55-61 15854548-11 2005 Low-dose imatinib, that induces complete hematological and molecular genetic remission, exerts significant effects on FIP1L1-PDGFRA positive HES. Imatinib Mesylate 9-17 factor interacting with PAPOLA and CPSF1 Homo sapiens 118-124 15700042-5 2005 Analysis of early tumour cell seeding by using [(125)I]iododeoxyuridine-labelled C26 cells or by in vivo microscopy showed that rh-E reduced tumour cell seeding in the liver sinusoids. Idoxuridine 55-71 factor interacting with PAPOLA and CPSF1 Homo sapiens 128-132 15621768-11 2004 Imatinib is an excellent candidate for first line treatment of Loeffler"s endocarditis, especially when the FIP1L1/PDGFA fusion gene is detected. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 108-114 15995324-9 2005 A subset of MCD patients with associated eosinophilia who carry the FIP1L1-PDGFRA oncogene will achieve complete clinical, histological, and molecular remissions with imatinib mesylate therapy, in contrast to those with c-kit D816V mutations. Imatinib Mesylate 167-184 factor interacting with PAPOLA and CPSF1 Homo sapiens 68-74 15567248-1 2004 Thaliblastine exhibits dose dependent cytotoxic effect on HL-60, HL-60/DOX, RHE and HD-MY-2 leukemia cells. thalicarpine 0-13 factor interacting with PAPOLA and CPSF1 Homo sapiens 76-79 16089297-3 2005 FIP1L1-PDGFR alpha is a novel therapeutic target of the kinase inhibitor imatinib (Glivec, Novartis), which provides the basis for the treatment of these patients with this drug. Imatinib Mesylate 73-81 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 16089297-4 2005 FIP1L1-PDGFRA positive CEL patients respond very well to imatinib therapy, some of which are remarkable responses with normalization of the blood counts within 2 weeks after start of the therapy. Imatinib Mesylate 57-65 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 16089297-6 2005 All imatinib treated FIP1L1-PDGFRA positive CEL patients achieve hematological and cytogenetic remission, and the majority of patients also achieve a molecular remission with the fusion gene no longer detectable in blood, even by the most sensitive PCR techniques. Imatinib Mesylate 4-12 factor interacting with PAPOLA and CPSF1 Homo sapiens 21-27 15500716-12 2004 The identification of FIP1L1-PDGFRA rearrangement is a useful molecular mark for HES diagnosis and works as the therapeutic target of imatinib. Imatinib Mesylate 134-142 factor interacting with PAPOLA and CPSF1 Homo sapiens 22-28 15455302-9 2004 CONCLUSION: Imatinib provides a potent therapeutic option in FIP1L1-PDGFRA negative patients suffering from HES. Imatinib Mesylate 12-20 factor interacting with PAPOLA and CPSF1 Homo sapiens 61-67 15284118-7 2004 Treatment with low-dose imatinib (100 mg/d) produced complete and durable responses in all 8 FIP1L1-PDGFRA(+) cases treated. Imatinib Mesylate 24-32 factor interacting with PAPOLA and CPSF1 Homo sapiens 93-99 15305431-2 2004 Beginning with the observation that imatinib mesylate (Gleevec) could elicit rapid and complete hematologic remissions in a proportion of patients with HES, a reverse bedside-to-bench translational research effort led to the discovery of FIP1L1-PDGFRA, a novel fusion gene on chromosome 4q12 whose product is an imatinib-sensitive protein tyrosine kinase. Imatinib Mesylate 36-53 factor interacting with PAPOLA and CPSF1 Homo sapiens 238-244 15339694-0 2004 Soft tissue and skeletal involvement in FIP1L1-PDGFR-alpha positive chronic eosinophilic leukemia: imatinib mesylate may induce complete molecular and imaging remission. Imatinib Mesylate 99-116 factor interacting with PAPOLA and CPSF1 Homo sapiens 40-46 15305431-2 2004 Beginning with the observation that imatinib mesylate (Gleevec) could elicit rapid and complete hematologic remissions in a proportion of patients with HES, a reverse bedside-to-bench translational research effort led to the discovery of FIP1L1-PDGFRA, a novel fusion gene on chromosome 4q12 whose product is an imatinib-sensitive protein tyrosine kinase. Imatinib Mesylate 36-44 factor interacting with PAPOLA and CPSF1 Homo sapiens 238-244 14749727-6 2004 hFip1, CPSF160 and PAP form a ternary complex in vitro, suggesting that hFip1 and CPSF160 act together in poly(A) site recognition and in cooperative recruitment of PAP to the RNA. Poly A 106-113 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-5 15036941-2 2004 Complete remissions, in response to treatment with low-dose imatinib mesylate (100 mg/day or less) have now been documented in all cases of FIP1L1-PDGFRA(+) eosinophilic disorder as well as other eosinophilic disorders that carry activation mutations of the PDGFRB gene that is located on chromosome 5q33. Imatinib Mesylate 60-77 factor interacting with PAPOLA and CPSF1 Homo sapiens 140-146 14973504-6 2004 Imatinib induced rapid complete hematological responses in 4/4 treated FIP1L1-PDGFRA (+) cases, including one female, and complete molecular remission in 2/3 evaluable cases. Imatinib Mesylate 0-8 factor interacting with PAPOLA and CPSF1 Homo sapiens 71-77 14973504-8 2004 Thus, correlating IHES/CEL genotype with phenotype, FIP1L1-PDGFRA (+) CEL emerges as a homogeneous clinicobiological entity, where imatinib can induce molecular remission. Imatinib Mesylate 131-139 factor interacting with PAPOLA and CPSF1 Homo sapiens 52-58 15175999-5 2004 Fusion of the Fip1-like 1 gene (FIP1L1) and the platelet-derived growth factor receptor alpha gene (PDGFRA) was discovered in the majority of patients with imatinib-sensitive HES, and all patients with the fusion responded to imatinib. Imatinib Mesylate 156-164 factor interacting with PAPOLA and CPSF1 Homo sapiens 14-25 15175999-5 2004 Fusion of the Fip1-like 1 gene (FIP1L1) and the platelet-derived growth factor receptor alpha gene (PDGFRA) was discovered in the majority of patients with imatinib-sensitive HES, and all patients with the fusion responded to imatinib. Imatinib Mesylate 156-164 factor interacting with PAPOLA and CPSF1 Homo sapiens 32-38 15175999-5 2004 Fusion of the Fip1-like 1 gene (FIP1L1) and the platelet-derived growth factor receptor alpha gene (PDGFRA) was discovered in the majority of patients with imatinib-sensitive HES, and all patients with the fusion responded to imatinib. Imatinib Mesylate 226-234 factor interacting with PAPOLA and CPSF1 Homo sapiens 14-25 15175999-5 2004 Fusion of the Fip1-like 1 gene (FIP1L1) and the platelet-derived growth factor receptor alpha gene (PDGFRA) was discovered in the majority of patients with imatinib-sensitive HES, and all patients with the fusion responded to imatinib. Imatinib Mesylate 226-234 factor interacting with PAPOLA and CPSF1 Homo sapiens 32-38 15175999-7 2004 The efficacy of relatively low imatinib concentrations in HES, mediated by inhibition of FIP1L1-PDGFRalpha kinase activity, causally implicates FIP1L1-PDGFRA in the pathogenesis in certain HES patients. Imatinib Mesylate 31-39 factor interacting with PAPOLA and CPSF1 Homo sapiens 89-95 15175999-7 2004 The efficacy of relatively low imatinib concentrations in HES, mediated by inhibition of FIP1L1-PDGFRalpha kinase activity, causally implicates FIP1L1-PDGFRA in the pathogenesis in certain HES patients. Imatinib Mesylate 31-39 factor interacting with PAPOLA and CPSF1 Homo sapiens 144-150 14973504-5 2004 In FIP1L1-PDGFRA (+) CEL, palpable splenomegaly was present in 5/8 cases, serum vitamin B(12) was always markedly increased, and marrow biopsies revealed a distinctively myeloproliferative aspect. Niacinamide 80-89 factor interacting with PAPOLA and CPSF1 Homo sapiens 3-9 14749727-6 2004 hFip1, CPSF160 and PAP form a ternary complex in vitro, suggesting that hFip1 and CPSF160 act together in poly(A) site recognition and in cooperative recruitment of PAP to the RNA. Poly A 106-113 factor interacting with PAPOLA and CPSF1 Homo sapiens 72-77 14757533-2 2004 Beginning with the observation that imatinib mesylate (Gleevec) could elicit rapid and complete hematologic remissions in a proportion of patients with HES, a reverse bedside-to-bench translational research effort led to the discovery of FIP1L1-PDGFRA, a novel fusion gene on chromosome 4q12 whose product is an imatinib-sensitive protein tyrosine kinase. Imatinib Mesylate 36-53 factor interacting with PAPOLA and CPSF1 Homo sapiens 238-244 15003901-0 2004 Imatinib mesylate can induce complete molecular remission in FIP1L1-PDGFR-a positive idiopathic hypereosinophilic syndrome. Imatinib Mesylate 0-17 factor interacting with PAPOLA and CPSF1 Homo sapiens 61-67 14757533-2 2004 Beginning with the observation that imatinib mesylate (Gleevec) could elicit rapid and complete hematologic remissions in a proportion of patients with HES, a reverse bedside-to-bench translational research effort led to the discovery of FIP1L1-PDGFRA, a novel fusion gene on chromosome 4q12 whose product is an imatinib-sensitive protein tyrosine kinase. Imatinib Mesylate 36-44 factor interacting with PAPOLA and CPSF1 Homo sapiens 238-244 12842979-7 2003 While all 3 patients with the FIP1L1-PDGFRA rearrangement achieved a sustained complete response with imatinib mesylate therapy, the other two, both carrying the c-kit Asp816 to Val (Asp816Val) mutation, did not. Imatinib Mesylate 102-119 factor interacting with PAPOLA and CPSF1 Homo sapiens 30-36 14676627-3 2004 Successful empiric treatment of patients with the hypereosinophilic syndrome with the selective tyrosine kinase inhibitor imatinib mesylate (Gleevec, Novartis) ultimately led to the discovery of the FIP1L1-PDGFRalpha fusion kinase in about half of the hypereosinophilic syndrome cases. Imatinib Mesylate 122-139 factor interacting with PAPOLA and CPSF1 Homo sapiens 199-205 14676627-6 2004 In vitro and in vivo studies confirmed that FIP1L1-PDGFRalpha is a therapeutic target of imatinib, forming a rational basis for the treatment of FIP1L1-PDGFRA positive chronic eosinophilic leukemia and mastocytosis with imatinib. Imatinib Mesylate 89-97 factor interacting with PAPOLA and CPSF1 Homo sapiens 44-50 14676627-6 2004 In vitro and in vivo studies confirmed that FIP1L1-PDGFRalpha is a therapeutic target of imatinib, forming a rational basis for the treatment of FIP1L1-PDGFRA positive chronic eosinophilic leukemia and mastocytosis with imatinib. Imatinib Mesylate 89-97 factor interacting with PAPOLA and CPSF1 Homo sapiens 145-151 14676627-6 2004 In vitro and in vivo studies confirmed that FIP1L1-PDGFRalpha is a therapeutic target of imatinib, forming a rational basis for the treatment of FIP1L1-PDGFRA positive chronic eosinophilic leukemia and mastocytosis with imatinib. Imatinib Mesylate 220-228 factor interacting with PAPOLA and CPSF1 Homo sapiens 44-50 14676627-6 2004 In vitro and in vivo studies confirmed that FIP1L1-PDGFRalpha is a therapeutic target of imatinib, forming a rational basis for the treatment of FIP1L1-PDGFRA positive chronic eosinophilic leukemia and mastocytosis with imatinib. Imatinib Mesylate 220-228 factor interacting with PAPOLA and CPSF1 Homo sapiens 145-151 14676628-6 2004 FIP1L1-PDGFRA+ mast cell disease responds completely to imatinib mesylate. Imatinib Mesylate 56-73 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 12842979-3 2003 Recently, a novel tyrosine kinase that is generated from fusion of the Fip1-like 1 (FIP1L1) and PDGFR alpha (PDGFRA) genes has been identified as a therapeutic target for imatinib mesylate in hypereosinophilic syndrome (HES). Imatinib Mesylate 171-179 factor interacting with PAPOLA and CPSF1 Homo sapiens 71-82 7675408-6 1995 Both maternal serum titers and AF bilirubin measurements provided early indications that the fetus might have the RhE antigen. Bilirubin 34-43 factor interacting with PAPOLA and CPSF1 Homo sapiens 114-117 12842979-3 2003 Recently, a novel tyrosine kinase that is generated from fusion of the Fip1-like 1 (FIP1L1) and PDGFR alpha (PDGFRA) genes has been identified as a therapeutic target for imatinib mesylate in hypereosinophilic syndrome (HES). Imatinib Mesylate 171-179 factor interacting with PAPOLA and CPSF1 Homo sapiens 84-90 8969812-2 1996 Enhancement of the therapeutic benefit of recombinant human erythropoietin (rhEp) in very-low-birth-weight infants will require a better understanding of rhEp"s pharmacodynamic effects including its interaction with iron in stimulating erythropoiesis. Iron 216-220 factor interacting with PAPOLA and CPSF1 Homo sapiens 76-80 8969812-3 1996 The purpose of this study was to determine the effects of chronic rhEp administration on plasma iron levels and hematopoiesis using a twin lamb model. Iron 96-100 factor interacting with PAPOLA and CPSF1 Homo sapiens 66-70 8969812-6 1996 During the rhEp treatment period, significantly greater negative daily AUCs were observed in the rhEp-treated lambs for plasma iron concentration (p = 0.0008), while significantly greater positive daily AUCs were observed for hemoglobin concentration (p = 0.04) and reticulocyte count (p = 0.02). Iron 127-131 factor interacting with PAPOLA and CPSF1 Homo sapiens 11-15 8969812-6 1996 During the rhEp treatment period, significantly greater negative daily AUCs were observed in the rhEp-treated lambs for plasma iron concentration (p = 0.0008), while significantly greater positive daily AUCs were observed for hemoglobin concentration (p = 0.04) and reticulocyte count (p = 0.02). Iron 127-131 factor interacting with PAPOLA and CPSF1 Homo sapiens 97-101 8969812-7 1996 In the rhEp-treated group, pretreatment iron concentrations were directly associated with the magnitude of the iron response during treatment such that the greater the pretreatment iron, the greater the daily AUC below the plasma iron concentration-time plot (r = -0.66, p = 0.05). Iron 40-44 factor interacting with PAPOLA and CPSF1 Homo sapiens 7-11 8969812-7 1996 In the rhEp-treated group, pretreatment iron concentrations were directly associated with the magnitude of the iron response during treatment such that the greater the pretreatment iron, the greater the daily AUC below the plasma iron concentration-time plot (r = -0.66, p = 0.05). Iron 111-115 factor interacting with PAPOLA and CPSF1 Homo sapiens 7-11 8969812-7 1996 In the rhEp-treated group, pretreatment iron concentrations were directly associated with the magnitude of the iron response during treatment such that the greater the pretreatment iron, the greater the daily AUC below the plasma iron concentration-time plot (r = -0.66, p = 0.05). Iron 111-115 factor interacting with PAPOLA and CPSF1 Homo sapiens 7-11 8969812-7 1996 In the rhEp-treated group, pretreatment iron concentrations were directly associated with the magnitude of the iron response during treatment such that the greater the pretreatment iron, the greater the daily AUC below the plasma iron concentration-time plot (r = -0.66, p = 0.05). Iron 111-115 factor interacting with PAPOLA and CPSF1 Homo sapiens 7-11 8969812-9 1996 These observations suggest that treatment of rapidly growing newborn lambs with rhEp results in increased iron utilization due to increased erythropoiesis and depends on iron status at the initiation of rhEp treatment. Iron 106-110 factor interacting with PAPOLA and CPSF1 Homo sapiens 80-84 8969812-9 1996 These observations suggest that treatment of rapidly growing newborn lambs with rhEp results in increased iron utilization due to increased erythropoiesis and depends on iron status at the initiation of rhEp treatment. Iron 170-174 factor interacting with PAPOLA and CPSF1 Homo sapiens 80-84 8969812-9 1996 These observations suggest that treatment of rapidly growing newborn lambs with rhEp results in increased iron utilization due to increased erythropoiesis and depends on iron status at the initiation of rhEp treatment. Iron 170-174 factor interacting with PAPOLA and CPSF1 Homo sapiens 203-207 12660384-0 2003 A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome. Imatinib Mesylate 94-102 factor interacting with PAPOLA and CPSF1 Homo sapiens 54-60 12660384-7 2003 FIP1L1-PDGFRalpha is a constitutively activated tyrosine kinase that transforms hematopoietic cells and is inhibited by imatinib (50 percent inhibitory concentration, 3.2 nM). Imatinib Mesylate 120-128 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 12660384-8 2003 The FIP1L1-PDGFRA fusion gene was subsequently detected in 9 of 16 patients with the syndrome and in 5 of the 9 patients with responses to imatinib that lasted more than three months. Imatinib Mesylate 139-147 factor interacting with PAPOLA and CPSF1 Homo sapiens 4-10 12660384-11 2003 The acquisition of a T674I resistance mutation at the time of relapse demonstrates that FIP1L1-PDGFRalpha is the target of imatinib. Imatinib Mesylate 123-131 factor interacting with PAPOLA and CPSF1 Homo sapiens 88-94 8504984-2 1993 In an effort to evaluate a possible role for human erythropoietin (rh-E) in preventing or minimizing carboplatin-induced anemia we analyzed the impact of the agent on anemia and transfusion requirements of women with ovarian cancer who were treated on one of two nonrandomized trials employing identical second-line carboplatin-based intraperitoneal regimens, with the only difference in the regimens being the addition of rh-E (Study 1, without rh-E; Study 2, with rh-E). Carboplatin 101-112 factor interacting with PAPOLA and CPSF1 Homo sapiens 67-71 7833484-4 1995 It is a C-->G transition at nucleotide position 676, which leads to an amino acid substitution from proline to alanine in the Rh e-carrying polypeptide. Proline 103-110 factor interacting with PAPOLA and CPSF1 Homo sapiens 129-133 7833484-4 1995 It is a C-->G transition at nucleotide position 676, which leads to an amino acid substitution from proline to alanine in the Rh e-carrying polypeptide. Alanine 114-121 factor interacting with PAPOLA and CPSF1 Homo sapiens 129-133 7833484-6 1995 In one polymerase chain reaction, the sense primer had a 3"-end nucleotide specific for the cytosine at position 676 of the Rh E allele. 3"-end nucleotide 57-74 factor interacting with PAPOLA and CPSF1 Homo sapiens 124-128 7833484-6 1995 In one polymerase chain reaction, the sense primer had a 3"-end nucleotide specific for the cytosine at position 676 of the Rh E allele. Cytosine 92-100 factor interacting with PAPOLA and CPSF1 Homo sapiens 124-128 7833484-7 1995 In another reaction, a sense primer was used with a 3"-end nucleotide specific for the guanine at position 676 of the Rh e allele and the Rh D gene, whereas the antisense primer had a 3"-end nucleotide specific for the adenine at position 787 of the Rh CcEe gene. 3"-end nucleotide 52-69 factor interacting with PAPOLA and CPSF1 Homo sapiens 118-122 7833484-7 1995 In another reaction, a sense primer was used with a 3"-end nucleotide specific for the guanine at position 676 of the Rh e allele and the Rh D gene, whereas the antisense primer had a 3"-end nucleotide specific for the adenine at position 787 of the Rh CcEe gene. Guanine 87-94 factor interacting with PAPOLA and CPSF1 Homo sapiens 118-122 7833484-10 1995 Thus, we may conclude that the ASPA approach leads to a simple and reliable method to determine the Rh E/e genotype. aspa 31-35 factor interacting with PAPOLA and CPSF1 Homo sapiens 100-104 7833484-12 1995 Moreover, our results confirm the proposed association between the cytosine/guanine polymorphism at position 676 and the Rh E/e phenotype. Cytosine 67-75 factor interacting with PAPOLA and CPSF1 Homo sapiens 121-125 7833484-12 1995 Moreover, our results confirm the proposed association between the cytosine/guanine polymorphism at position 676 and the Rh E/e phenotype. Guanine 76-83 factor interacting with PAPOLA and CPSF1 Homo sapiens 121-125 8504984-5 1993 In this nonrandomized comparison of two identical chemotherapy programs we have demonstrated that rh-E significantly reduced the incidence and severity of anemia associated with carboplatin-based chemotherapy. Carboplatin 178-189 factor interacting with PAPOLA and CPSF1 Homo sapiens 98-102 8504984-6 1993 A randomized trial examining the potential impact of rh-E on carboplatin-induced anemia and transfusion requirements is warranted. Carboplatin 61-72 factor interacting with PAPOLA and CPSF1 Homo sapiens 53-57 34717949-4 2022 Owing to the improved selectivity of ZnO, excellent conductivity of carbon fiber, promoted active site exposure and mass transfer of hollow structure, the free-standing membrane electrode shows superior 2e-WOR performances with high selectivity (83.8% at 2.8 V vs. RHE), H2O2 generation rate (19.7 mumol cm-2 min-1) and robust stability. Zinc Oxide 37-40 factor interacting with PAPOLA and CPSF1 Homo sapiens 265-268 33797222-8 2021 With the addition of IrOx cocatalyst, at 1.23 V (vs RHE), the heterojunction gave ~2 mA cm-2. irox cocatalyst 21-36 factor interacting with PAPOLA and CPSF1 Homo sapiens 52-55 34717949-4 2022 Owing to the improved selectivity of ZnO, excellent conductivity of carbon fiber, promoted active site exposure and mass transfer of hollow structure, the free-standing membrane electrode shows superior 2e-WOR performances with high selectivity (83.8% at 2.8 V vs. RHE), H2O2 generation rate (19.7 mumol cm-2 min-1) and robust stability. Carbon 68-74 factor interacting with PAPOLA and CPSF1 Homo sapiens 265-268 34643624-1 2021 A Ni-based MOF is in situ grown onto Ni(OH)2 nanosheets to effectively suppress the oxygen evolution reaction for the efficient electrocatalytic oxidation of biomass-derived 5-hydroxymethylfurfural to 2,5-furandicarboxylic acid with 100% yield and faradaic efficiency at 1.4 V (vs. RHE). nickel hydroxide 37-44 factor interacting with PAPOLA and CPSF1 Homo sapiens 282-285 34571305-3 2022 Interestingly, it has been found that when the 2D Fe-MNS catalyst was functionalized with visible-light-responsive (Ru(bpy))32+ as a dye-sensitizer, the electrons from the (Ru(bpy))32+ can effectively inject into the 2D Fe-MNS, which resulted in a negative shift of the LUMO potential of the 2D Fe-MNS to -0.15 V (vs. RHE). Echothiophate Iodide 47-49 factor interacting with PAPOLA and CPSF1 Homo sapiens 318-321 34571305-3 2022 Interestingly, it has been found that when the 2D Fe-MNS catalyst was functionalized with visible-light-responsive (Ru(bpy))32+ as a dye-sensitizer, the electrons from the (Ru(bpy))32+ can effectively inject into the 2D Fe-MNS, which resulted in a negative shift of the LUMO potential of the 2D Fe-MNS to -0.15 V (vs. RHE). fe-mns 50-56 factor interacting with PAPOLA and CPSF1 Homo sapiens 318-321 34571305-3 2022 Interestingly, it has been found that when the 2D Fe-MNS catalyst was functionalized with visible-light-responsive (Ru(bpy))32+ as a dye-sensitizer, the electrons from the (Ru(bpy))32+ can effectively inject into the 2D Fe-MNS, which resulted in a negative shift of the LUMO potential of the 2D Fe-MNS to -0.15 V (vs. RHE). (ru(bpy))32+ 115-127 factor interacting with PAPOLA and CPSF1 Homo sapiens 318-321 34571305-3 2022 Interestingly, it has been found that when the 2D Fe-MNS catalyst was functionalized with visible-light-responsive (Ru(bpy))32+ as a dye-sensitizer, the electrons from the (Ru(bpy))32+ can effectively inject into the 2D Fe-MNS, which resulted in a negative shift of the LUMO potential of the 2D Fe-MNS to -0.15 V (vs. RHE). (ru(bpy))32+ 172-184 factor interacting with PAPOLA and CPSF1 Homo sapiens 318-321 34571305-3 2022 Interestingly, it has been found that when the 2D Fe-MNS catalyst was functionalized with visible-light-responsive (Ru(bpy))32+ as a dye-sensitizer, the electrons from the (Ru(bpy))32+ can effectively inject into the 2D Fe-MNS, which resulted in a negative shift of the LUMO potential of the 2D Fe-MNS to -0.15 V (vs. RHE). fe-mns 220-226 factor interacting with PAPOLA and CPSF1 Homo sapiens 318-321 34571305-3 2022 Interestingly, it has been found that when the 2D Fe-MNS catalyst was functionalized with visible-light-responsive (Ru(bpy))32+ as a dye-sensitizer, the electrons from the (Ru(bpy))32+ can effectively inject into the 2D Fe-MNS, which resulted in a negative shift of the LUMO potential of the 2D Fe-MNS to -0.15 V (vs. RHE). 2d fe-mns 292-301 factor interacting with PAPOLA and CPSF1 Homo sapiens 318-321 34919376-6 2021 Owing to the strong adsorption of nitrate on Fe0 active sites generated via topotactic conversion and in situ electroreduction, 2D Fe-cyano electrocatalyst exhibits high catalytic activity with a yield rate of 42.1 mg h-1 mgcat-1 and a Faradaic efficiency of over 90% toward NH3 production at -0.5 V (vs reversible hydrogen electrode, RHE). Nitrates 34-41 factor interacting with PAPOLA and CPSF1 Homo sapiens 335-338 34919376-6 2021 Owing to the strong adsorption of nitrate on Fe0 active sites generated via topotactic conversion and in situ electroreduction, 2D Fe-cyano electrocatalyst exhibits high catalytic activity with a yield rate of 42.1 mg h-1 mgcat-1 and a Faradaic efficiency of over 90% toward NH3 production at -0.5 V (vs reversible hydrogen electrode, RHE). fe-cyano 131-139 factor interacting with PAPOLA and CPSF1 Homo sapiens 335-338 34919376-6 2021 Owing to the strong adsorption of nitrate on Fe0 active sites generated via topotactic conversion and in situ electroreduction, 2D Fe-cyano electrocatalyst exhibits high catalytic activity with a yield rate of 42.1 mg h-1 mgcat-1 and a Faradaic efficiency of over 90% toward NH3 production at -0.5 V (vs reversible hydrogen electrode, RHE). Ammonia 275-278 factor interacting with PAPOLA and CPSF1 Homo sapiens 335-338 34643624-1 2021 A Ni-based MOF is in situ grown onto Ni(OH)2 nanosheets to effectively suppress the oxygen evolution reaction for the efficient electrocatalytic oxidation of biomass-derived 5-hydroxymethylfurfural to 2,5-furandicarboxylic acid with 100% yield and faradaic efficiency at 1.4 V (vs. RHE). Oxygen 84-90 factor interacting with PAPOLA and CPSF1 Homo sapiens 282-285 34643624-1 2021 A Ni-based MOF is in situ grown onto Ni(OH)2 nanosheets to effectively suppress the oxygen evolution reaction for the efficient electrocatalytic oxidation of biomass-derived 5-hydroxymethylfurfural to 2,5-furandicarboxylic acid with 100% yield and faradaic efficiency at 1.4 V (vs. RHE). 5-hydroxymethylfurfural 174-197 factor interacting with PAPOLA and CPSF1 Homo sapiens 282-285 34643624-1 2021 A Ni-based MOF is in situ grown onto Ni(OH)2 nanosheets to effectively suppress the oxygen evolution reaction for the efficient electrocatalytic oxidation of biomass-derived 5-hydroxymethylfurfural to 2,5-furandicarboxylic acid with 100% yield and faradaic efficiency at 1.4 V (vs. RHE). 2,5-furandicarboxylic acid 201-227 factor interacting with PAPOLA and CPSF1 Homo sapiens 282-285 34164898-4 2021 The reconstructed amino-functionalized indium-based catalyst demonstrates a high Faradaic efficiency of 94.4% and a partial current density of 108 mA cm-2 at -1.1 V vs. RHE in a liquid-phase flow cell, and also delivers an enhanced current density of ~800 mA cm-2 at 3.4 V for the formate production in a gas-phase flow cell configuration. Indium 39-45 factor interacting with PAPOLA and CPSF1 Homo sapiens 169-172 34554733-5 2021 The us-HEA/C achieves an ultrahigh mass activity of 28.3 A mg-1noble metals at -0.05 V (vs the reversible hydrogen electrode, RHE) for HER in 0.5 M H2SO4 solution, which is 40.4 and 74.5 times higher than those of the commercial Pt/C and Rh/C catalysts, respectively. Hydrogen 106-114 factor interacting with PAPOLA and CPSF1 Homo sapiens 126-129 34554733-5 2021 The us-HEA/C achieves an ultrahigh mass activity of 28.3 A mg-1noble metals at -0.05 V (vs the reversible hydrogen electrode, RHE) for HER in 0.5 M H2SO4 solution, which is 40.4 and 74.5 times higher than those of the commercial Pt/C and Rh/C catalysts, respectively. sulfuric acid 148-153 factor interacting with PAPOLA and CPSF1 Homo sapiens 126-129 34304603-2 2021 FIP1L1-PDGFRA fusion ((Fip1-like 1-platelet-derived growth factor receptor alpha); F/P) leads to the proliferation of the eosinophilic lineage and thus to a clonal hypereosinophilic syndrome that is highly responsive to imatinib. Imatinib Mesylate 220-228 factor interacting with PAPOLA and CPSF1 Homo sapiens 0-6 34342137-5 2021 It is found that Cu@Ag-2 NPs with the proper thickness of Ag shell exhibit the Faradaic efficiency (FE) of total C2 products and ethylene as high as 67.6% and 32.2% at -1.1 V (versus reversible hydrogen electrode, RHE), respectively. Copper 17-19 factor interacting with PAPOLA and CPSF1 Homo sapiens 214-217 34342137-5 2021 It is found that Cu@Ag-2 NPs with the proper thickness of Ag shell exhibit the Faradaic efficiency (FE) of total C2 products and ethylene as high as 67.6% and 32.2% at -1.1 V (versus reversible hydrogen electrode, RHE), respectively. A(2)C 113-115 factor interacting with PAPOLA and CPSF1 Homo sapiens 214-217 34342137-5 2021 It is found that Cu@Ag-2 NPs with the proper thickness of Ag shell exhibit the Faradaic efficiency (FE) of total C2 products and ethylene as high as 67.6% and 32.2% at -1.1 V (versus reversible hydrogen electrode, RHE), respectively. ethylene 129-137 factor interacting with PAPOLA and CPSF1 Homo sapiens 214-217 35507543-3 2022 As the electrocatalyst used for the oxidation of benzyl alcohol, NiCo-61-MOF/NF presented a lower overpotential and superior chemical durability than other electrocatalysts; it only required a potential of ~1.52 V (vs RHE) to reach 338.16 mA cm-2, with an oxidation efficiency of more than 86%. Benzyl Alcohol 49-63 factor interacting with PAPOLA and CPSF1 Homo sapiens 218-221 34130448-4 2021 Consequently, the selectivity of the HNCS reaches ~91.9% at 0.7 V (vs RHE), and the output for H2O2 production is up to 618.5 mmol gcatalyst-1 h-1 in 0.1 M KOH solution. Hydrogen Peroxide 95-99 factor interacting with PAPOLA and CPSF1 Homo sapiens 70-73 34130448-4 2021 Consequently, the selectivity of the HNCS reaches ~91.9% at 0.7 V (vs RHE), and the output for H2O2 production is up to 618.5 mmol gcatalyst-1 h-1 in 0.1 M KOH solution. potassium hydroxide 156-159 factor interacting with PAPOLA and CPSF1 Homo sapiens 70-73 34179617-3 2021 Combining this catalysis reaction and common graphite paper, the lowest anodic potentials 0.63 V (vs RHE) and 1.09 V (vs RHE) were obtained for driving a 10 mA/cm2 current density in alkali and near-neutral seawater electrolytes, respectively, outperforming all the as-reported alkali or near-neutral seawater catalysts accordingly to the best of our knowledge. Graphite 45-53 factor interacting with PAPOLA and CPSF1 Homo sapiens 101-104 34179617-3 2021 Combining this catalysis reaction and common graphite paper, the lowest anodic potentials 0.63 V (vs RHE) and 1.09 V (vs RHE) were obtained for driving a 10 mA/cm2 current density in alkali and near-neutral seawater electrolytes, respectively, outperforming all the as-reported alkali or near-neutral seawater catalysts accordingly to the best of our knowledge. Graphite 45-53 factor interacting with PAPOLA and CPSF1 Homo sapiens 121-124 34430811-4 2021 Thin free-standing Si photoanodes with sub-50 mum thickness are demonstrated by incorporating a nickel oxide (NiOx) thin film as oxygen evolution catalyst, light-trapping surface structure, and a rear-pn+ junction, to generate a photo-current density of 23.43 mA/cm2 with an onset potential of 1.2 V (vs. RHE). si photoanodes 19-33 factor interacting with PAPOLA and CPSF1 Homo sapiens 305-308 34192868-3 2021 We reveal that these Ni-hG and Fe-hG catalysts can be combined in any proportion to produce a desired syngas ratio (1-10) across a wide potential range (-0.6 to -1.1 V vs RHE), required commercially for the Fischer-Tropsch (F-T) synthesis of liquid fuels and chemicals. ni-hg 21-26 factor interacting with PAPOLA and CPSF1 Homo sapiens 171-174 34192868-3 2021 We reveal that these Ni-hG and Fe-hG catalysts can be combined in any proportion to produce a desired syngas ratio (1-10) across a wide potential range (-0.6 to -1.1 V vs RHE), required commercially for the Fischer-Tropsch (F-T) synthesis of liquid fuels and chemicals. fe-hg 31-36 factor interacting with PAPOLA and CPSF1 Homo sapiens 171-174 35507543-4 2022 Besides, after continuous electrocatalysis for 20 000 s at 1.42 V (vs RHE), the current density of NiCo-61-MOF/NF nanosheets was still 38.67 mA cm-2 with 77.34% retention. Niacin 99-103 factor interacting with PAPOLA and CPSF1 Homo sapiens 70-73 35436090-3 2022 The dualism of N-dopants and binary metals lower the d-band centers of both Fe and Co in the Fe,Co,N-C catalyst, improving the overpotential of the overall electrocatalytic processes (DeltaEORR-OER = 0.74 +- 0.02 V vs RHE). Iron 76-78 factor interacting with PAPOLA and CPSF1 Homo sapiens 218-221 35522475-2 2022 Herein, PdFe 1 single-atom alloy metallene, in which the Fe single atoms are confined on Pd metallene support, is first developed as an effective and robust NRR electro catalyst, delivering the exceptional NRR performance with an NH 3 yield of 111.9 mug h -1 mg -1 , a Faradaic efficiency of 37.8 % at -0.2 V (RHE) , as well as a long-term stability for 100 h electrolysis . metallene 33-42 factor interacting with PAPOLA and CPSF1 Homo sapiens 310-313 35522475-2 2022 Herein, PdFe 1 single-atom alloy metallene, in which the Fe single atoms are confined on Pd metallene support, is first developed as an effective and robust NRR electro catalyst, delivering the exceptional NRR performance with an NH 3 yield of 111.9 mug h -1 mg -1 , a Faradaic efficiency of 37.8 % at -0.2 V (RHE) , as well as a long-term stability for 100 h electrolysis . Iron 57-59 factor interacting with PAPOLA and CPSF1 Homo sapiens 310-313 35522475-2 2022 Herein, PdFe 1 single-atom alloy metallene, in which the Fe single atoms are confined on Pd metallene support, is first developed as an effective and robust NRR electro catalyst, delivering the exceptional NRR performance with an NH 3 yield of 111.9 mug h -1 mg -1 , a Faradaic efficiency of 37.8 % at -0.2 V (RHE) , as well as a long-term stability for 100 h electrolysis . pd metallene 89-101 factor interacting with PAPOLA and CPSF1 Homo sapiens 310-313 35436090-3 2022 The dualism of N-dopants and binary metals lower the d-band centers of both Fe and Co in the Fe,Co,N-C catalyst, improving the overpotential of the overall electrocatalytic processes (DeltaEORR-OER = 0.74 +- 0.02 V vs RHE). Iron 93-95 factor interacting with PAPOLA and CPSF1 Homo sapiens 218-221 35436090-3 2022 The dualism of N-dopants and binary metals lower the d-band centers of both Fe and Co in the Fe,Co,N-C catalyst, improving the overpotential of the overall electrocatalytic processes (DeltaEORR-OER = 0.74 +- 0.02 V vs RHE). Cobalt 96-98 factor interacting with PAPOLA and CPSF1 Homo sapiens 218-221 35436090-3 2022 The dualism of N-dopants and binary metals lower the d-band centers of both Fe and Co in the Fe,Co,N-C catalyst, improving the overpotential of the overall electrocatalytic processes (DeltaEORR-OER = 0.74 +- 0.02 V vs RHE). Nitrogen 99-101 factor interacting with PAPOLA and CPSF1 Homo sapiens 218-221 35436090-3 2022 The dualism of N-dopants and binary metals lower the d-band centers of both Fe and Co in the Fe,Co,N-C catalyst, improving the overpotential of the overall electrocatalytic processes (DeltaEORR-OER = 0.74 +- 0.02 V vs RHE). Carbon 101-102 factor interacting with PAPOLA and CPSF1 Homo sapiens 218-221 35166553-4 2022 CO2 reduction performance tests indicate that an ordered nanoneedle array reaches a 59% Faraday efficiency for multicarbon products (FEC2) at -1.2 V (vs RHE), compared to a FEC2 of 20% for a disordered nanoneedle array (CuNNs). Carbon Dioxide 0-3 factor interacting with PAPOLA and CPSF1 Homo sapiens 153-156 35377140-4 2022 The oxide-derived PdIn surface has shown excellent eCO2RR activity and enhanced CO selectivity with a Faradaic efficiency (FE) of 92.13% at -0.9 V (vs RHE). Oxides 4-9 factor interacting with PAPOLA and CPSF1 Homo sapiens 151-154 35166553-4 2022 CO2 reduction performance tests indicate that an ordered nanoneedle array reaches a 59% Faraday efficiency for multicarbon products (FEC2) at -1.2 V (vs RHE), compared to a FEC2 of 20% for a disordered nanoneedle array (CuNNs). multicarbon products 111-131 factor interacting with PAPOLA and CPSF1 Homo sapiens 153-156