Search results for "TIP"

showing 10 items of 6351 documents

In silico identification of small molecules as new cdc25 inhibitors through the correlation between chemosensitivity and protein expression pattern

2021

The cell division cycle 25 (Cdc25) protein family plays a crucial role in controlling cell proliferation, making it an excellent target for cancer therapy. In this work, a set of small molecules were identified as Cdc25 modulators by applying a mixed ligand-structure-based approach and taking advantage of the correlation between the chemosensitivity of selected structures and the protein expression pattern of the proposed target. In the first step of the in silico protocol, a set of molecules acting as Cdc25 inhibitors were identified through a new ligand-based protocol and the evaluation of a large database of molecular structures. Subsequently, induced-fit docking (IFD) studies allowed us…

0301 basic medicineHepG2Protein familyCdc25In silicoAntiproliferative activityCell cycleLigandsCatalysisArticleInorganic Chemistrylcsh:Chemistry03 medical and health sciencesCdc250302 clinical medicineCDC2 Protein KinaseDrug DiscoveryHumanscdc25 PhosphatasesComputer SimulationMolecular Targeted TherapyPhysical and Theoretical ChemistryPhosphorylationMolecular Biologylcsh:QH301-705.5DRUDITSpectroscopyBinding SitesbiologyCell growthChemistryOrganic ChemistryGeneral MedicineHep G2 CellsCell cycleAntiproliferative activity; Cdc25; Cell cycle; DRUDIT; HepG2; Molecular dockingLigand (biochemistry)Small moleculeComputer Science Applications030104 developmental biologyBiochemistrylcsh:Biology (General)lcsh:QD1-999Docking (molecular)030220 oncology & carcinogenesisMolecular dockingbiology.proteinDrug Screening Assays Antitumor
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Hepatitis B Virus Subverts the Autophagy Elongation Complex Atg5-12/16L1 and Does Not Require Atg8/LC3 Lipidation for Viral Maturation

2018

ABSTRACT Previous studies indicated that hepatitis B virus (HBV) stimulates autophagy to favor its production. To understand how HBV co-opts autophagy as a proviral machinery, we studied the roles of key autophagy proteins in HBV-replicating liver cell cultures. RNA interference-mediated silencing of Atg5, Atg12, and Atg16L1, which promote autophagophore expansion and LC3 membrane conjugation, interfered with viral core/nucleocapsid (NC) formation/stability and strongly diminished virus yields. Concomitantly, the core/NC membrane association and their sorting to envelope-positive compartments were perturbed. A close inspection of the HBV/autophagy cross talk revealed that the virus depended…

0301 basic medicineHepatitis B virusATG8Autophagosome maturationImmunologyATG5Autophagy-Related ProteinsBiologymedicine.disease_causeVirus ReplicationMicrobiologyVirusAutophagy-Related Protein 5ATG1203 medical and health sciencesVirologyCell Line TumormedicineAutophagyHumansHepatitis B virusAutophagyAutophagy-Related Protein 8 FamilyHepatitis BCell biologyVirus-Cell Interactions030104 developmental biologyViral replicationInsect ScienceGene Knockdown TechniquesMultiprotein ComplexesMicrotubule-Associated ProteinsAutophagy-Related Protein 12
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Neonatal hyperinsulinemic hypoglycemia: case report of kabuki syndrome due to a novel KMT2D splicing-site mutation

2020

Abstract Background Persistent neonatal hypoglycemia, owing to the possibility of severe neurodevelopmental consequences, is a leading cause of neonatal care admission. Hyperinsulinemic hypoglycemia is often resistant to dextrose infusion and needs rapid diagnosis and treatment. Several congenital conditions, from single gene defects to genetic syndromes should be considered in the diagnostic approach. Kabuki syndrome type 1 (MIM# 147920) and Kabuki syndrome type 2 (MIM# 300867), can be associated with neonatal hyperinsulinemic hypoglycemia. Patient presentation We report a female Italian (Sicilian) child, born preterm at 35 weeks gestation, with persistent hypoglycemia. Peculiar facial dys…

0301 basic medicineHeterozygotePediatricsmedicine.medical_specialtyFacial dysmorphismNeonatal hypotoniaCase ReportHypoglycemiamedicine.disease_causeDiagnosis DifferentialNervous system malformation03 medical and health sciences0302 clinical medicineHyperinsulinismmedicineHumansAbnormalities MultipleHyperinsulinemic hypoglycemiaPathologicalbusiness.industryNeonatal hypoglycemiaInfant Newbornlcsh:RJ1-570lcsh:Pediatricsmedicine.diseaseHematologic DiseasesNeoplasm ProteinsDNA-Binding ProteinsPhenotype030104 developmental biologyNeonatal hypotoniaItalyVestibular DiseasesFaceMutationGestationFemalebusinessHyperinsulinismKabuki syndromeInfant PrematureNeonatal hypoglycemia030217 neurology & neurosurgeryItalian Journal of Pediatrics
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Autophagy interferes with human cytomegalovirus genome replication, morphogenesis, and progeny release.

2020

Viral infections are often accompanied by the induction of autophagy as an intrinsic cellular defense mechanism. Herpesviruses have developed strategies to evade autophagic degradation and to manipulate autophagy of the host cells to their benefit. Here we addressed the role of macroautophagy/autophagy in human cytomegalovirus replication and for particle morphogenesis. We found that proteins of the autophagy machinery localize to cytoplasmic viral assembly compartments and enveloped virions in the cytoplasm. Surprisingly, the autophagy receptor SQSTM1/p62 was also found to colocalize with HCMV capsids in the nucleus of infected cells. This finding indicates that the autophagy machinery int…

0301 basic medicineHuman cytomegalovirusCytoplasmEpstein-Barr Virus InfectionsvirusesCytomegalovirusBiology03 medical and health sciencesMultiplicity of infectionmedicineXenophagyAutophagyMorphogenesisHumansMolecular BiologyCytopathic effect030102 biochemistry & molecular biologyAutophagyCell BiologyBECN1biochemical phenomena metabolism and nutritionFibroblastsmedicine.diseaseVirus ReleaseCell biology030104 developmental biologyCytomegalovirus InfectionsMAP1LC3AResearch PaperAutophagy
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Molecular docking-based virtual drug screening revealing an oxofluorenyl benzamide and a bromonaphthalene sulfonamido hydroxybenzoic acid as HDAC6 in…

2020

HDAC6 is a crucial epigenetic modifier that plays a vital role in tumor progression and carcinogenesis due to its multiple biological functions. It is a unique member of class-II HDAC enzymes. It possesses two catalytic domains, which function independently of the overall enzyme activity. Up to date, there are only a few selective HDAC6 inhibitors with anti-cancer activity. In this study, 175,204 ligands obtained from the ZINC15 and OTAVAchemical databases were used for virtual drug screening against HDAC6. Molecular docking studies were performed for 100 selected compounds. Furthermore, the top 10 compounds obtained from docking were tested for their efficacy to inhibit the function of HDA…

0301 basic medicineHydroxybenzoic acidMicroscale thermophoresisDrug developmentApoptosisRM1-950NaphthalenesVirtual drug screeningHistone Deacetylase 6Flow cytometry03 medical and health scienceschemistry.chemical_compoundStructure-Activity Relationship0302 clinical medicineCell Line TumorDrug DiscoverymedicineHydroxybenzoatesHumansBenzamideCytotoxicityBenzoic acidCancerPharmacologychemistry.chemical_classificationLeukemiamedicine.diagnostic_testDose-Response Relationship DrugMolecular StructureChemistryMicroscale thermophoresisGeneral MedicineHDAC6Drug Resistance MultipleHistone Deacetylase InhibitorsMolecular Docking Simulation030104 developmental biologyEnzymeBiochemistryDocking (molecular)Drug Resistance Neoplasm030220 oncology & carcinogenesisBenzamidesEpigeneticsTherapeutics. PharmacologyDatabases ChemicalBiomedicinepharmacotherapy = Biomedecinepharmacotherapie
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Analysis of substrate binding in individual active sites of bifunctional human ATIC

2018

Aminoimidazolecarboxamide ribonucleotide formyl transferase (AICARFT): Inosine monophosphate cyclohydrolase (IMPCH, collectively called ATIC) is a bifunctional enzyme that catalyses the penultimate and final steps in the purine de novo biosynthesis pathway. The bifunctional protein is dimeric and each monomer contains two different active sites both of which are capable of binding nucleotide substrates, this means to a potential total of four distinct binding events might be observed. Within this work we used a combination of site-directed and truncation mutants of ATIC to independently investigate the binding at these two sites using calorimetry. A single S10W mutation is sufficient to blo…

0301 basic medicineHydroxymethyl and Formyl TransferasesModels MolecularRibonucleotideStereochemistryBiophysicsBiochemistryAnalytical ChemistrySubstrate Specificity03 medical and health scienceschemistry.chemical_compoundMultienzyme ComplexesCatalytic DomainTransferaseHumansNucleotidePhosphofructokinase 2Bifunctional enzymesMolecular Biologychemistry.chemical_classification030102 biochemistry & molecular biologybiologyNucleotidesActive siteCooperative bindingIsothermal titration calorimetryXanthosine monophosphate030104 developmental biologyBiochemistrychemistryNucleotide DeaminasesMultiple binding sitesbiology.proteinIsothermal titration calorimetryProtein Binding
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Synthesis, antitumor activity and CDK1 inhibiton of new thiazole nortopsentin analogues

2017

A new series of thiazole nortopsentin analogues was conveniently synthesized with fair overall yields. The antiproliferative activity of the new derivatives was tested against different human tumor cell lines of the NCI full panel. Four of them showed good antitumor activity with GI(50) values from micro to nanomolar level. The mechanism of the antiproliferative effect of these derivatives, was pro-apoptotic, being associated with externalization of plasma membrane phosphatidylserine and DNA fragmentation. The most active and selective of the new thiazoles confined viable cells in G2/M phase and markedly inhibited in vitro CDK1 activity. (C) 2017 Elsevier Masson SAS.

0301 basic medicineIndolesCell SurvivalStereochemistryMolecular ConformationNortopsentin analogues3-b]pyridinesAntineoplastic AgentsApoptosisMarine alkaloids Nortopsentin analogues Antiproliferative activity Apoptosis CDK1 inhibitors Thiazolyl-1H-pyrrolo[23-b]pyridinesAntiproliferative activity01 natural sciencesStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compoundMarine alkaloidsCDC2 Protein KinaseDrug DiscoveryHumansThiazoleProtein Kinase InhibitorsCell ProliferationPharmacologyCyclin-dependent kinase 1Dose-Response Relationship DrugMarine alkaloids; Nortopsentin analogues; Antiproliferative activity; Apoptosis; CDK1 inhibitors; Thiazolyl-1H-pyrrolo[2; 3-b]pyridines010405 organic chemistryOrganic ChemistryImidazolesGeneral MedicinePhosphatidylserineThiazolyl-1H-pyrrolo[2Settore CHIM/08 - Chimica FarmaceuticaCyclin-Dependent KinasesIn vitro0104 chemical sciencesCDK1 inhibitors030104 developmental biologyMembranechemistryCell cultureApoptosisMCF-7 CellsDNA fragmentationCaco-2 CellsDrug Screening Assays Antitumor
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Collective properties of viral infectivity

2018

Individual virions typically fail to infect cells. Such decoupling between virions and infectious units is most evident in multicomponent and other segmented viruses, but is also frequent in non-segmented viruses. Despite being a well-known observation, the causes and implications of low single-virion infectivity often remain unclear. In principle, this can originate from intrinsic genetic and/or structural virion defects, but also from host infection barriers that limit early viral proliferation. Hence, viruses may have evolved strategies to increase the per-virion likelihood of establishing successful infections. This can be achieved by adopting spread modes that elevate the multiplicity …

0301 basic medicineInfectivityvirusesBiologyVirus Physiological PhenomenaCellular levelbiochemical phenomena metabolism and nutritionVirus InternalizationVirus ReplicationVirologyMicrovesiclesDefective virusArticle03 medical and health sciences030104 developmental biologyMultiplicity of infectionViral replicationVirion bindingVirus DiseasesVirologyMicrobial InteractionsVirus Physiological Phenomena
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In vivo and in vitro effects of multiple sclerosis immunomodulatory therapeutics on glutamatergic excitotoxicity.

2015

In multiple sclerosis (MS), a candidate downstream mechanism for neuronal injury is glutamate (Glu)-induced excitotoxicity, leading to toxic increases in intraneuronal Ca(2+) . Here, we used in vivo two-photon imaging in the brain of TN-XXL transgenic Ca(2+) reporter mice to test whether promising oral MS therapeutics, namely fingolimod, dimethyl fumarate, and their respective metabolites fingolimod-phosphate and monomethyl fumarate, can protect neurons against acute glutamatergic excitotoxic damage. We also assessed whether these drugs can protect against excitotoxicity in vitro using primary cortical neurons, and whether they can directly inhibit Glu release from pathogenic T-helper 17 ly…

0301 basic medicineKainic acidMultiple SclerosisExcitotoxicityGlutamic AcidPharmacologyBiologymedicine.disease_causeBiochemistryNeuroprotectionImmunomodulation03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineIn vivomedicineAnimalsCells CulturedNeuronsKainic AcidDimethyl fumarateCell DeathGlutamate receptorNeurotoxicityBrainmedicine.diseaseUp-Regulation030104 developmental biologyNeuroprotective AgentschemistryNMDA receptor030217 neurology & neurosurgerySignal TransductionJournal of neurochemistry
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Conversion of the sensor kinase DcuS ofEscherichia coliof the DcuB/DcuS sensor complex to the C4-dicarboxylate responsive form by the transporter DcuB

2016

Summary The sensor kinase DcuS of Escherichia coli co-operates under aerobic conditions with the C4-dicarboxylate transporter DctA to form the DctA/DcuS sensor complex. Under anaerobic conditions C4-dicarboxylate transport in fumarate respiration is catalyzed by C4-dicarboxylate/fumarate antiporter DcuB. (i) DcuB interacted with DcuS as demonstrated by a bacterial two-hybrid system (BACTH) and by co-chromatography of the solubilized membrane-proteins (mHPINE assay). (ii) In the DcuB/DcuS complex only DcuS served as the sensor since mutations in the substrate site of DcuS changed substrate specificity of sensing, and substrates maleate or 3-nitropropionate induced DcuS response without affec…

0301 basic medicineKinaseAntiporter030106 microbiologyTransporterBiologymedicine.disease_causeMicrobiology03 medical and health sciencesBiochemistrySolubilizationmedicineSubstrate specificityEscherichia coliEcology Evolution Behavior and SystematicsEnvironmental Microbiology
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