Search results for "PROTEIN KINASE"

showing 10 items of 1188 documents

Down-Regulation of Ku Autoantigen, DNA-Dependent Protein Kinase, and Poly(ADP-ribose) Polymerase during Cellular Senescence

1997

During aging and cellular senescence mutations accumulate in genomic and mitochondrial DNA. Ku autoantigens, DNA-dependent protein kinase, and poly (ADP-ribose) polymerase have an essential role in DNA damage recognition. Our purpose was to find out whether cellular senescence of fibroblasts affects the protein components that recognize DNA damage and induce the repair process. We compared presenescent and replicatively senescent human WI-38 fibroblasts with each other and with SV-40 immortalized and serum-deficient quiescent WI-38 cells. Our results showed that replicative senescence significantly decreased the nuclear level of both p70 and p86 components of Ku autoantigen. SV-40 immortali…

SenescenceDNA damagePoly ADP ribose polymeraseMolecular Sequence DataBiophysicsDown-RegulationP70-S6 Kinase 1DNA FragmentationDNA-Activated Protein KinaseProtein Serine-Threonine KinasesAutoantigensBiochemistryCell LineDownregulation and upregulationHumansAmino Acid SequenceProtein kinase AKu AutoantigenLungMolecular BiologyCellular SenescencePolymerasebiologyDNA HelicasesNuclear ProteinsAntigens NuclearCell BiologyFibroblastsMolecular biologyDNA-Binding ProteinsApoptosisbiology.proteinPoly(ADP-ribose) PolymerasesBiochemical and Biophysical Research Communications
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Attenuation of NF-κB Signaling Response to UVB Light during Cellular Senescence

1999

The ability of cells to adapt to environmental stresses undergoes a progressive reduction during aging. NF-kappaB-mediated signaling is a major defensive system against various environmental challenges. The aim of this study was to find out whether replicative senescence affects the response of the NF-kappaB signaling pathway to UVB light in human WI-38 and IMR-90 fibroblasts. The exposure of early passage fibroblasts to UVB light inhibited the proliferation and induced a flat phenotype similar to that observed in replicatively senescent fibroblasts not exposed to UVB light. The UVB radiation dose used (153 mJ/cm2) did not induce apoptosis in either early or late passage WI-38 fibroblasts. …

SenescenceP50Ultraviolet RaysLactams MacrocyclicBiologyCell LineBenzoquinonesHumansEnzyme InhibitorsProtein Kinase InhibitorsCellular SenescenceCell Line TransformedNF-kappa BQuinonesCell BiologyFibroblastsTyrphostinsMolecular biologyIκBαRifabutinApoptosisPhosphorylationTumor necrosis factor alphaSignal transductionNuclear localization sequenceSignal TransductionExperimental Cell Research
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Proteomic analysis reveals a role for Bcl2-associated athanogene 3 and major vault protein in resistance to apoptosis in senescent cells by regulatin…

2014

Senescence is a prominent solid tumor response to therapy in which cells avoid apoptosis and instead enter into prolonged cell cycle arrest. We applied a quantitative proteomics screen to identify signals that lead to therapy-induced senescence and discovered that Bcl2-associated athanogene 3 (Bag3) is up-regulated after adriamycin treatment in MCF7 cells. Bag3 is a member of the BAG family of co-chaperones that interacts with Hsp70. Bag3 also regulates major cell-signaling pathways. Mass spectrometry analysis of the Bag3 Complex revealed a novel interaction between Bag3 and Major Vault Protein (MVP). Silencing of Bag3 or MVP shifts the cellular response to adriamycin to favor apoptosis. We…

SenescenceProteomicsCell cycle checkpointApoptosisBreast NeoplasmsBAG3BiochemistryAnalytical ChemistryMajor vault proteinCell Line TumorGene silencingHumansMolecular BiologyCellular SenescenceAdaptor Proteins Signal TransducingVault Ribonucleoprotein ParticlesMitogen-Activated Protein Kinase 1Antibiotics AntineoplasticMitogen-Activated Protein Kinase 3biologyResearchCell biologyApoptosisDoxorubicinbiology.proteinCancer researchSignal transductionApoptosis Regulatory ProteinsCell agingSignal TransductionMolecularcellular proteomics : MCP
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Differential expression pattern of the novel serine/threonine kinase, STK33, in mice and men

2005

Serine/threonine kinase 33 (STK33/Stk33) is a recently discovered gene whose inferred amino acid sequence translation displays characters typical for a calcium/calmodulin dependent kinase (CAMK). In this study we analysed the STK33/Stk33 RNA and protein distribution and the localization of the protein. The STK33/Stk33 expression pattern resembles those of some related members of the CAMK group. STK33/Stk33 displays a nonubiquitous and, in most tissues, low level of expression. It is highly expressed in testis, particularly in cells from the spermatogenic epithelia. Moreover, significant expression is detected in lung epithelia, alveolar macrophages, horizontal cells in the retina and in emb…

Serine/threonine-specific protein kinaseGSK-3Ca2+/calmodulin-dependent protein kinaseAKT1Cell Biologyc-RafBiologyMolecular BiologyBiochemistryMolecular biologyCAMKAKT3MAP2K7FEBS Journal
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The development of benzimidazoles as selective rho kinase inhibitors

2010

Rho Kinase (ROCK) is a serine/threonine kinase whose inhibition could prove beneficial in numerous therapeutic areas. We have developed a promising class of ATP-competitive inhibitors based upon a benzimidazole scaffold, which show excellent potency toward ROCK (IC(50)<10nM). This report details the optimization of selectivity for ROCK over other related kinases such as Protein kinase A (PKA).

Serine/threonine-specific protein kinaserho-Associated KinasesMAP kinase kinase kinaseChemistryKinaseOrganic ChemistryClinical BiochemistryPharmaceutical ScienceGlaucomaChromanMitogen-activated protein kinase kinaseBiochemistryBenzimidazoleBiochemistryDrug DiscoveryROCKMolecular MedicineBenzimidazolesCyclin-dependent kinase 9Protein kinase ARho KinaseProtein Kinase InhibitorsMolecular BiologyRho-associated protein kinaseProtein kinase CBioorganic & Medicinal Chemistry Letters : a tetrahedron publication for the rapid dissemination of preliminary communication and all aspects of bioorganic chemistry, medicinal chemistry and related disciplines
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EMBER—Embedding Multiple Molecular Fingerprints for Virtual Screening

2022

In recent years, the debate in the field of applications of Deep Learning to Virtual Screening has focused on the use of neural embeddings with respect to classical descriptors in order to encode both structural and physical properties of ligands and/or targets. The attention on embeddings with the increasing use of Graph Neural Networks aimed at overcoming molecular fingerprints that are short range embeddings for atomic neighborhoods. Here, we present EMBER, a novel molecular embedding made by seven molecular fingerprints arranged as different &ldquo;spectra&rdquo; to describe the same molecule, and we prove its effectiveness by using deep convolutional architecture that assesses ligands&…

Settore ING-INF/05 - Sistemi Di Elaborazione Delle InformazioniBinding SitesMolecular StructureDeep learning Drug design Embedding Virtual screeningResearchOrganic ChemistryGeneral MedicineLigandsCatalysisComputer Science ApplicationsInorganic ChemistryCDC2 Protein KinaseDrug DiscoveryMass Screeningdeep learning; drug design; virtual screening; embeddingNeural Networks ComputerPhysical and Theoretical ChemistryProtein KinasesMolecular BiologySpectroscopy
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Post-Transcriptional Regulation of Human Inducible Nitric-Oxide Synthase Expression by the Jun N-terminal Kinase

2007

Human inducible nitric-oxide synthase (iNOS) expression is regulated both at transcriptional and post-transcriptional levels. In the present study, the effect of Jun N-terminal kinase (JNK) on human iNOS expression was investigated. In A549/8 human alveolar epithelial cells, both the inhibition of JNK by a pharmacological inhibitor anthra[1,9-cd]pyrazol-6(2H)-one1,9-pyrazoloanthrone (SP600125) and small interfering RNA (siRNA)-mediated down-regulation of JNK led to a reduction of iNOS mRNA and protein expression. iNOS promoter activity was not affected by these treatments. Hence, JNK seems to regulate iNOS expression through post-transcriptional mechanisms by stabilizing iNOS mRNA. Our labo…

Small interfering RNARNA Stabilityp38 mitogen-activated protein kinasesDown-RegulationNitric Oxide Synthase Type IIRNA-binding proteinNitric Oxidep38 Mitogen-Activated Protein KinasesGene Expression Regulation EnzymologicCell LineTristetraprolinHumansPhosphorylationRNA Small InterferingPromoter Regions GeneticPost-transcriptional regulationAnthracenesPharmacologyRegulation of gene expressionMessenger RNAbiologyChemistryKinaseJNK Mitogen-Activated Protein KinasesEpithelial Cellsrespiratory systemMolecular biologyPulmonary AlveoliNitric oxide synthasebiology.proteinCytokinesMolecular MedicineSignal TransductionMolecular Pharmacology
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Response of yeast cells to high glucose involves molecular and physiological differences when compared to other osmostress conditions.

2015

Yeast cells can be affected by several causes of osmotic stress, such as high salt, sorbitol or glucose concentrations. The last condition is particularly interesting during natural processes where this microorganism participates. Response to osmostress requires the HOG (High Osmolarity Glycerol) pathway and several transcription factors, including Hot1, which plays a key role in high glucose concentrations. In this work, we describe how the yeast response to osmotic stress shows differences in accordance with the stress agent responsible for it. Compared with other conditions, under high glucose stress, delocalization of MAPK (Mitogen-Activated Protein Kinase) Hog1 is slower, induction of …

Snf3Saccharomyces cerevisiae ProteinsOsmotic shockTranscription GeneticSaccharomyces cerevisiaeChitinSaccharomyces cerevisiaeOsmosisApplied Microbiology and BiotechnologyMicrobiologychemistry.chemical_compoundOsmotic PressureGene Expression Regulation FungalSorbitolProtein kinase AbiologyGlycogenEthanolBenzenesulfonatesOsmolar ConcentrationGeneral Medicinebiology.organism_classificationYeastDNA-Binding ProteinsRepressor ProteinsBasic-Leucine Zipper Transcription FactorsGlucosechemistryBiochemistrySorbitolMitogen-Activated Protein KinasesTranscription FactorsFEMS yeast research
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Molecular mechanisms of sorafenib action in liver cancer cells.

2012

Sorafenib, a multikinase inhibitor, recently received FDA approval for the treatment of advanced hepatocellular carcinoma (HCC). However, as the clinical application of sorafenib evolves, there is increasing interest in defining the mechanisms underlying its anti-tumor activity. Considering that this specific inhibitor could target unexpected molecules depending on the biologic context, a precise understanding of its mechanism of action could be critical to maximize its treatment efficacy, while minimizing adverse effects. Two human HCC cell lines (HepG2 and Huh7), carrying different biological and genetic characteristics, were used in this study to examine the intracellular events leading …

SorafenibDNA ReplicationNiacinamideCarcinoma HepatocellularDNA RepairTranscription GeneticAngiogenesisCell SurvivalPyridinesApoptosisPharmacologyBiologysorafenib HCC mini-chromosome maintenance genes Dickkopf1 Harakiri Acheron/LARP6 YAP1 cell cycle microarray global gene expression analysisCell Line TumormedicineCell AdhesionHumansneoplasmsMolecular BiologyProtein Kinase InhibitorsCell ProliferationYAP1Neovascularization PathologicCell growthGene Expression ProfilingPhenylurea CompoundsBenzenesulfonatesCell CycleLiver NeoplasmsBiological TransportCell BiologyCell cycleSorafenibmedicine.diseasedigestive system diseasesMechanism of actionHepatocellular carcinomaProtein Biosynthesismedicine.symptomMitogen-Activated Protein KinasesLiver cancerDevelopmental Biologymedicine.drugSignal Transduction
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BIBF 1120/ nintedanib : a new triple angiokinase inhibitor-directed therapy in patients with non-small cell lung cancer.

2013

Abstract: Introduction: Several new targeted agents with anti-angiogenic properties have been developed recently, including vandetanib, sunitinib, sorafenib, bevacizumab and others. Tumor development, progression, metastasis are strongly linked to angiogenesis. Targeted agents like bevacizumab, a monoclonal antibody which targets VEGF, have been fully developed in several solid tumors. These new agents strongly advocate that targeting angiogenesis is one of the best approaches for cancer therapy. Areas covered: Those agents that target additional pro-angiogenic intracellular signaling pathways beyond VEGF signaling have also the potential to contribute to anticancer therapies. The authors p…

SorafenibIndolesLung NeoplasmsBevacizumabSettore MED/06 - Oncologia MedicaAngiogenesis InhibitorsPharmacologyVandetanibMetastasischemistry.chemical_compoundCarcinoma Non-Small-Cell LungmedicineAnimalsHumansPharmacology (medical)Lung cancerProtein Kinase InhibitorsPharmacologyNeovascularization Pathologicbusiness.industrySunitinibPharmacology. Therapyanti-angiogenesis BIBF 1120 nintedanib non-small cell lung cancer vascular endothelial growth factorGeneral MedicineProtein-Tyrosine Kinasesmedicine.diseaseVascular endothelial growth factorchemistryCancer researchNintedanibbusinessmedicine.drugExpert opinion on investigational drugs
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