Search results for "I3"

showing 10 items of 278 documents

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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Show me your signaling– and I’ll tell you who you are

2009

See Article, pages 725–733Cancer research and therapy have come a long way:the field started out in search of a ‘‘magic bullet” accord-ing to Paul Ehrlich’s theory, and was hoping to identifya target which was pivotal to signaling survival in trans-formed cells. Indeed, certain diseases with monocausalmutations were identified, and targeting of the muta-tional products has helped in the design of treatmentstrategies. In chronic myeloid leukemia (CML), the con-stitutive activation of the tyrosine kinase BCR-ABL ispathognomonic [1], and multiple BCR-ABL kinaseinhibitors (e.g. imatinib mesylate, dasatinib, nilotinib)have been developed and successfully used in the treat-ment of CML offering near-…

SorafenibMAPK/ERK pathwayHepatologybusiness.industryPharmacologyDasatinibImatinib mesylateNilotinibmedicineCancer researchErlotinibbusinessTyrosine kinasePI3K/AKT/mTOR pathwaymedicine.drugJournal of Hepatology
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Targeted therapy for hepatocellular carcinoma: novel agents on the horizon.

2012

Hepatocellular carcinoma (HCC) is the most common liver cancer, accounting for 90% of primary liver cancers. In the last decade it has become one of the most frequently occurring tumors worldwide and is also considered to be the most lethal of the cancer systems, accounting for approximately one third of all malignancies. Although the clinical diagnosis and management of early-stage HCC has improved significantly, HCC prognosis is still extremely poor. Furthermore, advanced HCC is a highly aggressive tumor with a poor or no response to common therapies. Therefore, new effective and well-tolerated therapy strategies are urgently needed. Targeted therapies have entered the field of anti-neopl…

SorafenibOncologymedicine.medical_specialtyPathologyCarcinoma Hepatocellularmedicine.medical_treatmentReviewsAntineoplastic AgentsDiseasesignal transduction inhibitorsModels BiologicalTargeted therapyInternal medicinemedicineCarcinomacancerAnimalsHumansMolecular Targeted TherapyHCCneoplasmsCause of deathbusiness.industryTherapies InvestigationalLiver NeoplasmsCancerDrugs Investigationalmedicine.diseasetargeted therapyVEGFdigestive system diseasesOncologyHepatocellular carcinomaRas/Raf/MEK/ERKHCC targeted therapy VEGF Ras/Raf/MEK/ERK PI3K/Akt/PTEN/mTOR signal transduction inhibitors cancPI3K/Akt/PTEN/mTORLiver cancerbusinessmedicine.drugSignal Transduction
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Defects induced by He+ irradiation in γ-Si3N4

2021

International audience; Formation and evolution of defect levels in the electronic structure of silicon nitride with cubic spinel structure, -Si 3 N 4 , after the irradiation with He + ions was investigated using spectroscopic techniques. Strong changes of cathodoluminescence (CL), photoluminescence (PL), photoluminescence excitation (PLE) and Raman spectra were detected. In particular, excitonic PL was significantly inhibited and a new near-IR band appeared with the band gap excitation h≥E g =5.05 eV. This was explained by an effective trapping of photoinduced electrons and holes by charged defects. The spectral shift of PL with the excitation photon energy indicated heterogeneous nature…

Spinel Si3N4PhotoluminescenceMaterials scienceBand gapExcitonCathodoluminescenceBiophysicsCathodoluminescence02 engineering and technologyElectronic structureengineering.material010402 general chemistry01 natural sciencesBiochemistryHe+ irradiation[SPI.MAT]Engineering Sciences [physics]/Materialssymbols.namesakeCondensed Matter::Materials SciencePhotoluminescence excitation[PHYS.COND]Physics [physics]/Condensed Matter [cond-mat]PhotoluminescenceStructural defectsComputingMilieux_MISCELLANEOUSSpinelGeneral Chemistry[CHIM.MATE]Chemical Sciences/Material chemistry021001 nanoscience & nanotechnologyCondensed Matter PhysicsAtomic and Molecular Physics and Optics0104 chemical sciencesCrystallographyengineeringsymbols[PHYS.COND.CM-MS]Physics [physics]/Condensed Matter [cond-mat]/Materials Science [cond-mat.mtrl-sci]0210 nano-technologyRaman spectroscopy
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New therapies for sepsis: focus on the interleukin (IL)12 family member IL27

2007

Sepsis is a severe complication of abdominal infections such as peritonitis and is associated with high mortality. Unfortunately, the molecular mechanisms controlling the development of sepsis are still incompletely understood. Interestingly, the interleukin (IL) 12 family member IL27 seems to play a key role in sepsis. In a murine model of septic peritonitis induced by caecal ligation and puncture (CLP), IL27 levels were found to be strongly induced. Furthermore, mice deficient for the EBI3 subunit of IL27 were resistant to CLP-induced septic peritonitis as compared to wild-type controls. This effect could be suppressed by injection of recombinant IL27. Further studies demonstrated that IL…

T-LymphocytesImmunologyPeritonitisPeritonitisGeneral Biochemistry Genetics and Molecular BiologySepsisMiceRheumatologySepsismedicineAnimalsHumansImmunology and AllergyInterleukin 27business.industryInterleukin-17InterleukinCell DifferentiationEBI3medicine.diseaseBlockadeDisease Models AnimalImmunologyInterleukin 12ImmunotherapyInterleukin 17Reactive Oxygen SpeciesbusinessSupplementAnnals of the Rheumatic Diseases
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Disruption of T helper 2-immune responses in Epstein–Barr virus-induced gene 3-deficient mice

2002

Epstein–Barr virus-induced gene 3 (EBI3) is a widely expressed IL-12p40-related protein that associates as a heterodimer with either IL-12p35 or an IL-12p35 homologue, p28, to create a new cytokine (IL-27). To define the function of EBI3in vivo, we generated knockout mice in which theebi3gene was targeted by homologous recombination. EBI3−/−mice exhibited normal numbers of both naive and mature CD4+and CD8+T cells and B cells, but markedly decreased numbers of invariant natural killer T cells (iNKT) as defined by staining with an α-galactosylceramide (αGalCer)-loaded CD1d-tetramer. iNKT cells from EBI3−/−mice exhibited decreased IL-4 and, to a lesser extent, IFN-γ production after αGalCer s…

T-Lymphocytesmedicine.medical_treatmentStimulationBiologyMinor Histocompatibility AntigensInterferon-gammaMiceTh2 CellsImmune systemmedicineAnimalsInterferon gammaReceptors CytokineInterleukin 4GlycoproteinsMultidisciplinaryInterleukinsEBI3Biological SciencesNatural killer T cellMolecular biologyMice Inbred C57BLCytokineImmunologyInterleukin-4CD8medicine.drugProceedings of the National Academy of Sciences
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T Cells Integrate Local and Global Cues to Discriminate between Structurally Similar Antigens

2015

International audience; T lymphocytes' ability to discriminate between structurally related antigens has been attributed to the unique signaling properties of the T cell receptor. However, recent studies have suggested that the output of this discrimination process is conditioned by environmental cues. Here, we demonstrate how the IL-2 cytokine, collectively generated by strongly activated T cell clones, can induce weaker T cell clones to proliferate. We identify the PI3K pathway as being critical for integrating the antigen and cytokine responses and for controlling cell-cycle entry. We build a hybrid stochastic/deterministic computational model that accounts for such signal synergism and …

T-Lymphocytesmedicine.medical_treatmentT cellEFFECTORMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyLYMPHOCYTESArticleGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokineACTIVATIONMicePhosphatidylinositol 3-KinasesAntigenmedicineAnimalsAntigenslcsh:QH301-705.5Sensory cuePI3K/AKT/mTOR pathwayAFFINITYIL-2T-cell receptorMEMORYPROLIFERATIONRECOGNITIONCell biologyMice Inbred C57BLCytokinemedicine.anatomical_structureDIFFERENTIATIONlcsh:Biology (General)ImmunologyCytokinesInterleukin-2Signal transductionTCRSignal Transduction
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Cutting Edge: A Key Pathogenic Role of IL-27 in T Cell- Mediated Hepatitis

2007

Abstract The signals driving T cell activation in T cell-mediated fulminant hepatitis are not fully understood. In this study, we identify the cytokine IL-27p28/EBI3 as a major pathogenic factor in the ConA model of T cell-mediated hepatitis. We found an up-regulation of hepatic EBI3 and p28 expression and augmented levels of IL-27 in wild-type mice after ConA administration, suggesting a potential pathogenic role of this cytokine in ConA hepatitis. Consistently, IL-27 EBI3-deficient mice were almost completely protected from ConA-induced liver damage. Such protection was associated with reduced levels of IFN-γ and its signaling proteins pSTAT-1 and T-bet. Finally, in vivo blockade of IL-27…

T-Lymphocytesmedicine.medical_treatmentT cellImmunologychemical and pharmacologic phenomenaBiologyMinor Histocompatibility AntigensInterferon-gammaMiceConcanavalin AmedicineAnimalsImmunology and AllergyReceptors CytokineReceptorFulminant hepatitisMice KnockoutHepatitisLiver injuryInterleukin-17EBI3medicine.diseaseUp-RegulationSTAT1 Transcription FactorCytokinemedicine.anatomical_structureImmunologyChemical and Drug Induced Liver InjurySignal transductionSignal TransductionThe Journal of Immunology
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A Regulatory Mechanism Involving TBP-1/Tat-Binding Protein 1 and Akt/PKB in the Control of Cell Proliferation

2011

Abstract TBP-1 /Tat-Binding Protein 1 (also named Rpt-5, S6a or PSMC3) is a multifunctional protein, originally identified as a regulator of HIV-1-Tat mediated transcription. It is an AAA-ATPase component of the 19S regulative subunit of the proteasome and, as other members of this protein family, fulfils different cellular functions including proteolysis and transcriptional regulation. We and others reported that over expression of TBP-1 diminishes cell proliferation in different cellular contexts with mechanisms yet to be defined. Accordingly, we demonstrated that TBP-1 binds to and stabilizes the p14ARF oncosuppressor increasing its anti-oncogenic functions. However, TBP-1 restrains cell…

TBP-1/Tat-Binding Protein 1lcsh:Medicinemacromolecular substancesBiologymTORC2Cell GrowthTBP-1/Tat-Binding Protein 1; cell proliferationp14arfMolecular Cell BiologyGeneticsCancer GeneticsTranscriptional regulationGene Networkslcsh:ScienceBiologyProtein kinase BPI3K/AKT/mTOR pathwayMultidisciplinaryCell growthAKTBinding proteinlcsh:RMolecular biologySignaling CascadesCell biologyTBP-1enzymes and coenzymes (carbohydrates)cell proliferationbiology.proteinMdm2lcsh:QCell DivisionResearch ArticleSignal TransductionPLoS ONE
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Sustained activation of mTOR pathway in embryonic neural stem cells leads to development of tuberous sclerosis complex-associated lesions

2011

SummaryTuberous Sclerosis Complex (TSC) is a multisystem genetic disorder characterized by hamartomatous neurological lesions that exhibit abnormal cell proliferation and differentiation. Hyperactivation of mTOR pathway by mutations in either the Tsc1 or Tsc2 gene underlies TSC pathogenesis, but involvement of specific neural cell populations in the formation of TSC-associated neurological lesions remains unclear. We deleted Tsc1 in Emx1-expressing embryonic telencephalic neural stem cells (NSCs) and found that mutant mice faithfully recapitulated TSC neuropathological lesions, such as cortical lamination defects and subependymal nodules (SENs). These alterations were caused by enhanced gen…

Telencephaloncongenital hereditary and neonatal diseases and abnormalitiesCellular differentiationNeuroepithelial CellsEmbryonic DevelopmentBiologyTuberous Sclerosis Complex 1 Proteinmurine modelCerebral VentriclesMiceNeural Stem CellsCell MovementTuberous SclerosismedicineGeneticsAnimalsAnimals; Animals Newborn; Cell Differentiation; Cell Movement; Cell Proliferation; Cerebral Ventricles; Embryonic Development; Embryonic Stem Cells; Epilepsy; Gene Silencing; Gene Targeting; Megalencephaly; Mice; Mutation; Neural Stem Cells; Neuroepithelial Cells; Neurons; TOR Serine-Threonine Kinases; Telencephalon; Tuberous Sclerosis; Tuberous Sclerosis Complex 1 Protein; Tumor Suppressor Proteins; Signal TransductionGene SilencingNeural cellPI3K/AKT/mTOR pathwayEmbryonic Stem CellsCell ProliferationNeuronsEpilepsymTOR; Neural Stem Cells; Tuberous Sclerosis; murine modelTOR Serine-Threonine KinasesTumor Suppressor ProteinsCell DifferentiationCell BiologyNewbornEmbryonic stem cellNeural stem cellMegalencephalyCell biologynervous system diseasesNeuroepithelial cellmedicine.anatomical_structureAnimals NewbornImmunologyGene TargetingMutationmTORMolecular MedicineTSC1TSC2Signal Transduction
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