Search results for "Proto-oncogene"

showing 10 items of 770 documents

RNAi mediated acute depletion of Retinoblastoma protein (pRb) promotes aneuploidy in human primary cells via micronuclei formation

2009

BACKGROUND: Changes in chromosome number or structure as well as supernumerary centrosomes and multipolar mitoses are commonly observed in human tumors. Thus, centrosome amplification and mitotic checkpoint dysfunctions are believed possible causes of chromosomal instability. The Retinoblastoma tumor suppressor (RB) participates in the regulation of synchrony between DNA synthesis and centrosome duplication and it is involved in transcription regulation of some mitotic genes. Primary human fibroblasts were transfected transiently with short interfering RNA (siRNA) specific for human pRb to investigate the effects of pRb acute loss on chromosomal stability. RESULTS: Acutely pRb-depleted fibr…

Small interfering RNAMitosisCell Cycle ProteinsProtein Serine-Threonine KinasesRetinoblastoma ProteinAurora KinasesRNA interferenceChromosomal InstabilityProto-Oncogene ProteinsChromosome instabilitymedicineHumansCentrosome duplicationRNA Small Interferinglcsh:QH573-671MitosisCells CulturedCell NucleusCentrosomebiologylcsh:CytologyRetinoblastomaRetinoblastoma proteinCell BiologyFibroblastsAneuploidymedicine.diseaseCell biologyCentrosomeRNAi Aneuploidy pRBRb anauploidybiology.proteinRNA Interferencebiological phenomena cell phenomena and immunityResearch ArticleBMC Cell Biology
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TRAIL-induced apoptosis of hepatocellular carcinoma cells is augmented by targeted therapies

2009

AIM: To analyze the effect of chemotherapeutic drugs and specific kinase inhibitors, in combination with the death receptor ligand tumor necrosis factor-related apoptosis inducing ligand (TRAIL), on overcoming TRAIL resistance in hepatocellular carcinoma (HCC) and to study the efficacy of agonistic TRAIL antibodies, as well as the commitment of antiapoptotic BCL-2 proteins, in TRAIL-induced apoptosis. METHODS: Surface expression of TRAIL receptors (TRAIL-R1-4) and expression levels of the antiapoptotic BCL-2 proteins MCL-1 and BCL-xL were analyzed by flow cytometry and Western blotting, respectively. Knock-down of MCL-1 and BCL-xL was performed by transfecting specific small interfering RNA…

SorafenibCarcinoma Hepatocellularbcl-X ProteinBcl-xLAntineoplastic AgentsApoptosisTNF-Related Apoptosis-Inducing Ligandchemistry.chemical_compoundCell Line TumormedicineAnimalsHumansLY294002Viability assayEnzyme InhibitorsPI3K/AKT/mTOR pathwaybiologyKinaseLiver NeoplasmsGastroenterologyGeneral Medicinedigestive system diseasesReceptors TNF-Related Apoptosis-Inducing LigandchemistryProto-Oncogene Proteins c-bcl-2ApoptosisDoxorubicinCancer researchbiology.proteinMyeloid Cell Leukemia Sequence 1 ProteinTumor necrosis factor alphaOriginal ArticleFluorouracilmedicine.drug
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What links BRAF to the heart function? new insights from the cardiotoxicity of BRAF inhibitors in cancer treatment

2015

The RAS-related signalling cascade has a fundamental role in cell. It activates differentiation and survival. It is particularly important one of its molecules, B-RAF. B-RAF has been a central point for research, especially in melanoma. Indeed, it lacked effective therapeutic weapons since the early years of its study. Molecules targeting B-RAF have been developed. Nowadays, two classes of molecules are approved by FDA. Multi-target molecules, such as Sorafenib and Regorafenib, and selective molecules, such as Vemurafenib and Dabrafenib. Many other molecules are still under investigation. Most of them are studied in phase 1 trials. Clinical studies correlate B-RAF inhibitors and QT prolonga…

SorafenibProto-Oncogene Proteins B-rafB-RAF inhibitorscardio-oncologySkin NeoplasmscardiotoxicityAntineoplastic AgentsReviewB-RAF inhibitorPharmacologyQT intervalSudden cardiac deathchemistry.chemical_compoundRegorafenibmedicineAnimalsHumansMolecular Targeted TherapydabrafenibVemurafenibMelanomaProtein Kinase InhibitorsCardiotoxicityClinical Trials as Topicbusiness.industryMelanomaB-RAFDabrafenibArrhythmias CardiacHeartmedicine.diseaseOncologychemistryCancer researchbusinessmedicine.drugSignal TransductionOncotarget
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Sarcophytolide: a new neuroprotective compound from the soft coral Sarcophyton glaucum

1998

Abstract Bioactivity-guided fractionation of an alcohol extract of the soft coral Sarcophyton glaucum collected from the intertidal areas and the fringing coral reefs near Hurghada, Red Sea, Egypt resulted in the isolation of a new lactone cembrane diterpene, sarcophytolide. The structure of this compound was deduced from its spectroscopic data and by comparison of the spectral data with those of known closely related cembrane-type compounds. In antimicrobial assays, the isolated compound exhibited a good activity towards Staphylococcus aureus, Pseudomonas aeruginosa , and Saccharomyces cerevisiae. Sarcophytolide was found to display a strong cytoprotective effect against glutamate-induced …

Staphylococcus aureusProgrammed cell deathSecondary metaboliteToxicologyNeuroprotectionCnidariaMicechemistry.chemical_compoundmedicineAnimalsRats WistarGlutamate receptorNeurotoxicityBiological activitymedicine.diseaseMolecular biologyRatsNeuroprotective AgentsProto-Oncogene Proteins c-bcl-2chemistryBiochemistryNMDA receptorCalciumDiterpenesDiterpenemedicine.drugToxicology
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Antiproliferative properties and g-quadruplex-binding of symmetrical naphtho[1,2-b:8,7-b’]dithiophene derivatives

2021

Background: G-quadruplex (G4) forming sequences are recurrent in telomeres and promoter regions of several protooncogenes. In normal cells, the transient arrangements of DNA in G-tetrads may regulate replication, transcription, and translation processes. Tumors are characterized by uncontrolled cell growth and tissue invasiveness and some of them are possibly mediated by gene expression involving G-quadruplexes. The stabilization of G-quadruplex sequences with small molecules is considered a promising strategy in anticancer targeted therapy. Methods: Molecular virtual screening allowed us identifying novel symmetric bifunctionalized naphtho[1,2-b:8,7-b’]dithiophene ligands as interesting ca…

StereochemistryPharmaceutical ScienceAntineoplastic AgentsNaphthols010402 general chemistryG-quadruplex01 natural sciencesArticleAnalytical ChemistryHeLaProto-Oncogene Proteins c-mycchemistry.chemical_compoundSynthesisQD241-441Transcription (biology)H-TeloG-QuadruplexDrug DiscoveryC-MYCHumansheterocyclic compoundsPhysical and Theoretical ChemistryAntiproliferative effect; C-MYC; G-Quadruplex; H-Telo; Molecular docking; Planar heterocyclic scaffold; SynthesisCell ProliferationAntiproliferative effectVirtual screeningbiology010405 organic chemistryCell growthChemistryCytotoxinsOrganic Chemistrybiology.organism_classificationSmall moleculeSettore CHIM/08 - Chimica FarmaceuticaIn vitro0104 chemical sciencesG-QuadruplexesPlanar heterocyclic scaffoldChemistry (miscellaneous)Settore CHIM/03 - Chimica Generale E InorganicaMolecular dockingMolecular MedicineDNAHeLa Cells
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Interplay of three G‑quadruplex units in the KIT promoter

2019

The proto-oncogene KIT encodes for a tyrosine kinase receptor, which is a clinically validated target for treating gastrointestinal stromal tumors. The KIT promoter contains a G-rich domain within a relatively long sequence potentially able to form three adjacent G-quadruplex (G4) units, namely, K2, SP, and K1. These G4 domains have been studied mainly as single quadruplex units derived from short truncated sequences and are currently considered promising targets for anticancer drugs, alternatively to the encoded protein. Nevertheless, the information reported so far does not contemplate the interplay between those neighboring G4s in the context of the whole promoter, possibly thwarting dru…

Stromal cellbiologyChemistryGeneral ChemistryG-quadruplexBiochemistryMolecular biologyProto-Oncogene MasCatalysisReceptor tyrosine kinaseG‐Quadruplex Multiple G4 cancerG-QuadruplexesProto-Oncogene Proteins c-kitColloid and Surface ChemistrySettore CHIM/03 - Chimica Generale E Inorganicabiology.proteinHumansPromoter Regions GeneticGene
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Focal DNA Copy Number Changes in Neuroblastoma Target MYCN Regulated Genes

2013

Neuroblastoma is an embryonic tumor arising from immature sympathetic nervous system cells. Recurrent genomic alterations include MYCN and ALK amplification as well as recurrent patterns of gains and losses of whole or large partial chromosome segments. A recent whole genome sequencing effort yielded no frequently recurring mutations in genes other than those affecting ALK. However, the study further stresses the importance of DNA copy number alterations in this disease, in particular for genes implicated in neuritogenesis. Here we provide additional evidence for the importance of focal DNA copy number gains and losses, which are predominantly observed in MYCN amplified tumors. A focal 5 kb…

TRANSCRIPTIONAL TARGETNeuroblastoma/geneticsPsychologie appliquéeMedizinlcsh:MedicineChromosomal DisordersNeuroblastoma0302 clinical medicineRGS Proteins/geneticsGene duplicationMolecular Cell BiologyBasic Cancer ResearchTUMOR-SUPPRESSORALK KINASElcsh:ScienceNeurological TumorsGeneticsRegulation of gene expressionOncogene Proteins0303 health sciencesN-Myc Proto-Oncogene ProteinACTIVATING MUTATIONSMultidisciplinaryCancer Risk FactorsHomozygoteChromosomal Deletions and DuplicationsNuclear ProteinsGenomicsSciences bio-médicales et agricolesSignaling in Selected DisciplinesCANCEROncogene Proteins/geneticsGene Expression Regulation NeoplasticOncology030220 oncology & carcinogenesisMedicineRNA Long NoncodingBiologieResearch ArticleSignal TransductionEXPRESSIONDNA Copy Number VariationsGenetic Causes of CancerDown-RegulationGenomicsBiologyMolecular Genetics03 medical and health sciencesGenome Analysis ToolsNeuroblastomaCell Line TumormicroRNAmedicineGeneticsCancer GeneticsHumansGene RegulationGeneneoplasmsBiology030304 developmental biologyOncogenic SignalingN-MYCTHERAPEUTIC TARGETRECEPTORMICRORNAlcsh:RBiology and Life SciencesChromosomeCancers and NeoplasmsHuman Geneticsmedicine.diseaseNuclear Proteins/geneticsMicroRNAs/geneticsMicroRNAsPediatric Oncologylcsh:QGenome Expression AnalysisN-MycRGS ProteinsPLoS ONE
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JNK phosphorylation relieves HDAC3-dependent suppression of the transcriptional activity of c-Jun

2003

The AP-1 transcription factor c-Jun is a prototypical nuclear effector of the JNK signal transduction pathway. The integrity of JNK phosphorylation sites at serines 63/73 and at threonines 91/93 in c-Jun is essential for signal-dependent target gene activation. We show that c-Jun phosphorylation mediates dissociation of an inhibitory complex, which is associated with histone deacetylase 3 (HDAC3). The subsequent events that ultimately cause increased mRNA synthesis are independent of c-Jun phosphorylation and its interaction with JNK. These findings provide an 'activation by de-repression' model as an explanation for the stimulatory function of JNK on c-Jun.

ThreonineTranscriptional ActivationTranscription GeneticMAP Kinase Kinase 4Proto-Oncogene Proteins c-junRecombinant Fusion ProteinsMitogen-activated protein kinase kinaseHistone DeacetylasesGeneral Biochemistry Genetics and Molecular BiologyCell LinePhosphorylation cascadeMiceSuppression GeneticGenes ReporterSerineAnimalsHumansRNA MessengerPhosphorylationMolecular BiologyTranscription factorSequence DeletionMitogen-Activated Protein Kinase KinasesGeneral Immunology and MicrobiologybiologyGeneral Neurosciencec-junJNK Mitogen-Activated Protein KinasesArticles3T3 CellsHDAC3Molecular biologyProtein Structure TertiaryMitogen-activated protein kinaseMutationMutagenesis Site-Directedbiology.proteinPhosphorylationSignal transductionProtein BindingThe EMBO Journal
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Ras, Rap, and Rac Small GTP-binding Proteins Are Targets for Clostridium sordellii Lethal Toxin Glucosylation

1996

Lethal toxin (LT) from Clostridium sordellii is one of the high molecular mass clostridial cytotoxins. On cultured cells, it causes a rounding of cell bodies and a disruption of actin stress fibers. We demonstrate that LT is a glucosyltransferase that uses UDP-Glc as a cofactor to covalently modify 21-kDa proteins both in vitro and in vivo. LT glucosylates Ras, Rap, and Rac. In Ras, threonine at position 35 was identified as the target amino acid glucosylated by LT. Other related members of the Ras GTPase superfamily, including RhoA, Cdc42, and Rab6, were not modified by LT. Incubation of serum-starved Swiss 3T3 cells with LT prevents the epidermal growth factor-induced phosphorylation of m…

ThreonineUridine Diphosphate GlucoseRHOABacterial ToxinsMolecular Sequence DataClostridium sordelliimacromolecular substancesCDC42GTPaseBiologyCell morphologyBiochemistryGTP PhosphohydrolasesProto-Oncogene Proteins p21(ras)MiceGTP-binding protein regulatorsGTP-Binding ProteinsAnimalsHumansAmino Acid SequenceMolecular BiologyClostridiumEpidermal Growth FactorKinase3T3 CellsCell Biologybiology.organism_classificationMolecular biologyActinsrac GTP-Binding ProteinsActin CytoskeletonKineticsGlucoserap GTP-Binding ProteinsGlucosyltransferasesCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinPhosphorylationGuanosine TriphosphateHeLa CellsJournal of Biological Chemistry
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pRb suppresses camptothecin-induced apoptosis in human osteosarcoma Saos-2 cells by inhibiting c-Jun N-terminal kinase

2001

AbstractThis paper studies the cytotoxic effect induced by the topoisomerase I inhibitor camptothecin in human osteosarcoma Saos-2 cells, which lack p53 and contain a non-functional form of the product of the retinoblastoma gene, pRb. Cytotoxicity induced by camptothecin was dose- and time-dependent; the treatment with 100 nM camptothecin reduced cell viability by 50% at 32 h and by 75% at 72 h of exposure. The cytotoxic effect was caused by apoptosis, as ascertained by morphological evidence, acridine orange-ethidium bromide staining and flow cytometric analysis. Apoptosis was accompanied by both the activation of caspase-3 and the fragmentation of poly(ADP-ribose) polymerase. Treatment wi…

Time FactorsCell SurvivalProto-Oncogene Proteins c-junBlotting WesternBiophysicsApoptosisBiologyTransfectionRetinoblastoma ProteinBiochemistryStructural BiologyTumor Cells CulturedpRb JNK topoisomerase I inhibitors osteosarcomaGeneticsmedicineHumansCytotoxic T cellViability assayPhosphorylationFragmentation (cell biology)neoplasmsMolecular BiologySaos-2 cellsc-Jun N-terminal kinaseCell SizeDose-Response Relationship DrugCaspase 3Cell growthCell Cyclec-junJNK Mitogen-Activated Protein KinasesHydrogen PeroxideCell BiologyFlow CytometryGlutathioneMolecular biologyEnzyme ActivationOxidative StresspRbDNA Topoisomerases Type IApoptosisCaspasesCamptothecinMitogen-Activated Protein KinasesPoly(ADP-ribose) PolymerasesTopoisomerase I InhibitorsCamptothecinmedicine.drugFEBS Letters
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