|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Cellular immunity to viral antigens lmits EL-deleted adenoviruses for gene therapy显示文摘 | Yang Y Nunes FA Berencsi K | 1994 | Proc Natl Acad Sci1994，91，： | 1 |
| 2 | Cellular immunity to viral antigens limits E1-deleted adenoviruses for gene therapy显示文摘 | Yang Y Nunes FA Berencsi K | 1994 | Proc Natl Acad Sci USA1994，91，： | 1 |
| 3 | Cellular immunity to viral antigens limits El-deleted adenoviruses for gene therapy显示文摘 | Yang Y Nunes FA Berencsi K | 1994 | Proc Natl Avad Svi USA1994，91，10： | 1 |
| 4 | Cellular immunity to viral antigens limits EI-deleted adenoviruses for gene therapy 显示文摘 | Yang Y Nunes FA Berencsi K | 1994 | Proc Natl Acad Sci USA1994，91，10： | 1 |
| 5 | Cellular immunity to viral antigens limits E1-deleted adenoviruses for gene therapy显示文摘 | Yang Y Nunes FA Rerencsi K | 1994 | Proc Natl Acad Sci USA1994，91，： | 1 |
| 6 | Cellular immunity to viral antigen limits El deleted adenoviruses for gene therapy显示文摘 | Yang Y Nunes FA Berencsi K | 1994 | Pro Natl Acad Sci USA1994，91，： | 1 |
| 7 | Gene transfer in- to the liver of nonhuman primates with E1 -deleted recombi- nant adenoviral vectors : safety of readministration 显示文摘 | Nunes FA Furth EE Wilson JM | 1999 | Hum Gene Ther1999，10，15： | 1 |
| 8 | Combination therapy with lami- vudine and adenovirus causes transient suppression of chronic woodchuck hepatitis B virus infections 显示文摘 | Zhou T Guo JT Nunes FA | 2000 | J Virol2000，74，11： | 1 |
| 9 | Effects of aerobic training on psychosocial morbidity and symptoms in patients with asthma: a randomized clinical trial 显示文摘 | Mendes FA Gonalves RC Nunes MP | 2010 | Chest2010，138，2： | 1 |
| 10 | Cellular immunity to viral antigens limits E1B-deleted adenoviruses for gene therapy显示文摘 | Yang Y Nunes FA Berencsi K | 1994 | Proc Natl Acad Sci U S A1994，91，10： | 1 |
| 11 | CelluIar immunity to viral antigens limits El-deleted adenoviruses for gene therapy 显示文摘 | Yang Y Nunes FA Berencsi K | 1999 | Proc Natl Acad Sci1999，91，10： | 1 |
| 12 | Assessment of liver function:pre-and peritransplant evaluation显示文摘 | Shaked A Nunes FA Olthoff KM | 1997 | Clin Chem1997，43，82： | 1 |
| 13 | Cellular immunity to viral antigens limits El-deleted adenovirus for gene therapy 显示文摘 | Nunes FA Bernencsi K | 1994 | Proc Natl Acad Sci USA1994，91，10： | 1 |
| 14 | Inactivation of E2a in recombination adenoviruses improves the prospect for gene therapy in cystic fibrosis显示文摘 | Yang Y Nunes FA Berencsi K | 1994 | Nature Genet1994，7，： | 1 |
| 15 | Cellular immunity to viral antigens limits El-deleted adenoviruses for gene therapy 显示文摘 | Yang Y Nunes FA Berencsi K | 1994 | Proc Natl Acad Sci1994，91，10： | 1 |
| 16 | In silico evidence of Remdesivir action in blood coagulation cascade modulation in COVID-19 treatment显示文摘BACKGROUND Coronavirus disease 2019(COVID-19)has demonstrated several clinical manifestations which include not only respiratory system issues but also liver,kidney,and other organ injuries.One of these abnormalities is coagulopathies,including thrombosis and disseminated intravascular coagulation.Because of this,the administration of low molecular weight heparin is required for patients that need to be hospitalized.In addition,Remdesivir is an antiviral that was used against Middle East Acute Respiratory Syndrome,Ebola,Acute Respiratory Syndrome,and other diseases,showing satisfactory results on recovery.Besides,there is evidence suggesting that this medication can provide a better prognosis for patients with COVID-19.AIM To investigate in silico the interaction between Remdesivir and clotting factors,pursuing a possibility of using it as medicine.METHODS In this in silico study,the 3D structures of angiotensin-converting enzyme 2(ACE2),Factor I(fibrinogen),Factor II(prothrombin),Factor III(thromboplastin),Factor V(proaccelerin),Factor VII(proconvertin),Factor VIII(antihemophilic factor A),Factor IX(antihemophilic factor B),Factor X(Stuart-Prower factor),and Factor XI(precursor of thromboplastin(these structures are technically called receptors)were selected from the Protein Data Bank.The structures of the antivirals Remdesivir and Osetalmivir(these structures are called ligands)were selected from the PubChem database,while the structure of Atazanavir was selected from the ZINC database.The software AutoDock Tools(ADT)was used to prepare the receptors for molecular docking.Ions,peptides,water molecules,and other ones were removed from each ligand,and then,hydrogen atoms were added to the structures.The grid box was delimited and calculated using the same software ADT.A physiological environment with pH 7.4 is needed to make the ligands interact with the receptors,and still the software Marvin sketch®(ChemAxon®)was used to forecast the protonation state.To perform molecular docking,ADT and Vina software was connected.Using PyMol®software and Discovery studio®software from BIOVIA,it was possible to analyze the amino acid residues from receptors that were involved in the interactions with the ligands.Ligand tortions,atoms that participated in the interactions,and the type,strength,and duration of the interactions were also analyzed using those software.RESULTS Molecular docking analysis showed that Remdesivir and ACE2 had an affinity energy of-8.8 kcal/moL,forming a complex with eight hydrogen bonds involving seven atoms of Remdesivir and five amino acid residues of ACE2.Remdesivir and prothrombin had an interaction with six hydrogen bonds involving atoms of the drug and five amino acid residues of the clotting factor.Similar to that,Remdesivir and thromboplastin presented interactions via seven hydrogen bonds involving five atoms of the drug and four residues of the clotting factor.While Remdesivir and Factor V established a complex with seven hydrogen bonds between six antiviral atoms and six amino acid residues from the factor,and Factor VII connected with the drug by four hydrogen bonds,which involved three atoms of the drug and three residues of amino acids of the factor.The complex between Remdesivir and Factor IX formed an interaction via 11 hydrophilic bonds with seven atoms of the drug and seven residues of the clotting factor,plus one electrostatic bond and three hydrophobic interactions.Factor X and Remdesivir had an affinity energy of-9.6 kcal/moL,and the complex presented 10 hydrogen bonds and 14 different hydrophobic interactions which involved nine atoms of the drug and 16 amino acid residues of the clotting factor.The interaction between Remdesivir and Factor XI formed five hydrogen bonds involving five amino acid residues of the clotting factor and five of the antiviral atoms.CONCLUSION Because of the in silico significant affinity,Remdesivir possibly could act in the severe acute respiratory syndrome coronavirus 2 infection blockade by interacting with ACE2 and concomitantly act in the modulation of the coagulation cascade preventing the hypercoagulable state. | Luis Gustavo Pagliarin Lucca Miketen de Oliveira Valentina Nunes Fontoura dos Anjos Cristiano de Bem Torquato de Souza Gabrielle Caroline Peiter Cinthia Façanha Wendel Anderson Dillmann Groto Fabrício Freire de Melo Kádima Nayara Teixeira | 2023 | World Journal of Biological Chemistry2023，14，4： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员