Search results for "Factor D"

showing 10 items of 48 documents

Estudio de acetilación de proteínas en líneas celulares humanas de cáncer colorectal KRAS mutado y salvaje

2016

El estado mutacional de KRAS es el principal predictor negativo de respuesta a terapias anti-factor de crecimiento epidérmico (EGFR) en pacientes diagnosticados de cáncer colorectal avanzado (CRC). Sin embargo existe datos contradictorios sobre las causas de la respuesta variable a estos fármacos diana de acuerdo con la presencia de mutaciones, de hecho publicaciones recientes han presentado datos no concluyentes sobre los pacientes portadores de mutaciones en el codón 13. En nuestro trabajo, hemos estudiado el impacto de la presencia de mutaciones en KRAS en proteínas intracelulares no histónicas. Para ello hemos utilizado diferentes líneas celulares de cáncer colorectal portadoras de dife…

Líneas celularesCancer ColorectalAcetilación proteícaKRASFármacos anti factor de crecimiento epidérmico
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Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2.

2006

International audience; Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. TRAIL-induced apoptosis is mediated by the transmembrane receptors death receptor 4 (DR4) (also known as TRAIL-R1) and DR5 (TRAIL-R2). TRAIL can also bind decoy receptor 1 (DcR1) (TRAIL-R3) and DcR2 (TRAIL-R4) that fail to induce apoptosis since they lack and have a truncated cytoplasmic death domain, respectively. In addition, DcR1 and DcR2 inhibit DR4- and DR5-mediated, TRAIL-induced apoptosis and we demonstrate here that this occurs through distinct mechanisms. While DcR1 prevents the assembly of the…

MESH : Hela CellsMESH: Membrane GlycoproteinsMESH: Membrane MicrodomainsDecoy Receptor 1ApoptosisMESH : Membrane GlycoproteinsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandJurkat Cells0302 clinical medicineMESH : Tumor Necrosis Factor Decoy ReceptorsMESH: Jurkat CellsDecoy receptorsReceptorCells CulturedMESH : Jurkat CellsMESH : Tumor Necrosis Factor-alpha0303 health sciencesMembrane GlycoproteinsMESH : Protein BindingArticlesMESH : Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsTumor Necrosis Factor Receptor-Associated Peptides and ProteinsCell biology030220 oncology & carcinogenesisCaspasesDeath-inducing signaling complexApoptosis/drug effects; Apoptosis Regulatory Proteins/antagonists & inhibitors; Apoptosis Regulatory Proteins/pharmacology; Caspases/metabolism; Cells Cultured; Death Domain Receptor Signaling Adaptor Proteins; Enzyme Activation/drug effects; GPI-Linked Proteins; HeLa Cells; Humans; Jurkat Cells; Membrane Glycoproteins/antagonists & inhibitors; Membrane Glycoproteins/pharmacology; Membrane Microdomains/drug effects; Protein Binding/drug effects; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor/metabolism; TNF-Related Apoptosis-Inducing Ligand; Tumor Necrosis Factor Decoy Receptors; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins/metabolism; Tumor Necrosis Factor-alpha/antagonists & inhibitors; Tumor Necrosis Factor-alpha/pharmacologyMESH : Apoptosis Regulatory ProteinsMESH: TNF-Related Apoptosis-Inducing LigandProtein BindingMESH: Cells CulturedDeath Domain Receptor Signaling Adaptor ProteinsMESH: Enzyme ActivationBiologyMESH: Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsGPI-Linked Proteins03 medical and health sciencesMembrane MicrodomainsCell surface receptorMESH : Cells Cultured[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyReceptors Tumor Necrosis Factor Member 10cHumansMESH: Protein Binding[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing LigandMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyDeath domainMESH: CaspasesMESH: HumansTumor Necrosis Factor-alphaMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell BiologyMESH: Receptors Tumor Necrosis FactorMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : Receptors Tumor Necrosis FactorEnzyme ActivationMESH: Hela CellsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsApoptosisMESH: Tumor Necrosis Factor-alphaMESH : Membrane MicrodomainsMESH : CaspasesApoptosis Regulatory ProteinsMESH : Enzyme ActivationMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy ReceptorsHeLa CellsMESH: Death Domain Receptor Signaling Adaptor Proteins
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Chemotherapy overcomes TRAIL-R4-mediated TRAIL resistance at the DISC level

2011

International audience; TNF-related apoptosis-inducing ligand or Apo2L (Apo2L/TRAIL) is a promising anti-cancer drug owing to its ability to trigger apoptosis by binding to TRAIL-R1 or TRAIL-R2, two membrane-bound receptors that are often expressed by tumor cells. TRAIL can also bind non-functional receptors such as TRAIL-R4, but controversies still exist regarding their potential to inhibit TRAIL-induced apoptosis. We show here that TRAIL-R4, expressed either endogenously or ectopically, inhibits TRAIL-induced apoptosis. Interestingly, the combination of chemotherapeutic drugs with TRAIL restores tumor cell sensitivity to apoptosis in TRAIL-R4-expressing cells. This sensitization, which ma…

MESH: CASP8 and FADD-Like Apoptosis Regulating ProteinMESH : Antineoplastic Combined Chemotherapy ProtocolsCASP8 and FADD-Like Apoptosis Regulating ProteinTRAILApoptosisMESH : Models BiologicalMitochondrionMESH : RNA Small InterferingMESH: Caspase 8TNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandMESH : Tumor Necrosis Factor Decoy Receptors0302 clinical medicineRNA interferenceNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsMESH: RNA Small InterferingMESH: NeoplasmsRNA Small InterferingReceptorSensitizationCaspase 80303 health sciencesMESH : Caspase 8MESH: Drug Resistance Neoplasm3. Good healthCell biologyMESH: Antineoplastic Combined Chemotherapy ProtocolsMESH : Drug Resistance Neoplasmmedicine.anatomical_structure030220 oncology & carcinogenesisRNA InterferenceMESH : GPI-Linked ProteinsMESH: TNF-Related Apoptosis-Inducing LigandDeath Domain Receptor Signaling Adaptor ProteinsProgrammed cell deathMESH: Cell Line Tumorc-FLIPMESH: RNA InterferenceBiologyGPI-Linked ProteinsCaspase 8Models Biological03 medical and health sciencesCell Line TumorReceptors Tumor Necrosis Factor Member 10cmedicineTRAIL-R4HumanscancerChemotherapy[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing Ligand[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyMolecular Biology030304 developmental biologyOriginal PaperMESH: HumansMESH : Cell Line TumorMESH: ApoptosisMESH : HumansMESH: Models BiologicalMESH : CASP8 and FADD-Like Apoptosis Regulating ProteinCell BiologyMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : NeoplasmsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsDrug Resistance NeoplasmApoptosisMESH : RNA InterferenceMESH: GPI-Linked ProteinsMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsMESH: Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy Receptors
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Effect of in vivo stimulation of mice on the secretion of factor B of the alternative complement pathway by peritoneal macrophages

1977

After in vivo treatment of mice with thioglycollate medium, the amount of native factor B which could be detected in vitro in culture supernatants of peritoneal macrophages was much lower than that found in supernatants of macrophages taken from untreated mice. However, when the macrophages from thioglycollate medium-treated mice were cultured on a plastic surface covered with glutardialdehyde-linked bovine serum albumin, the culture supernatants contained larger quantities of native factor B than culture supernatants of macrophages from untreated mice under the same conditions. Thus, the effect of in vivo thioglycollate medium treatment on the in vitro secretion of factor B by peritoneal m…

MacrophagesGuinea PigsImmunologyCell CountSerum Albumin BovineStimulationComplement System ProteinsBiologyComplement factor BIn vitroMicrobiologyMiceGlutaralIn vivobiology.proteinAlternative complement pathwayAnimalsImmunology and AllergySecretionFactor DBovine serum albuminPlasticsCells CulturedEuropean Journal of Immunology
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Adenoviral RB2/p130 gene transfer inhibits smooth muscle cell proliferation and prevents restenosis after angioplasty.

1999

Abstract —Smooth muscle cell (SMC) proliferation that results in neointima formation is implicated in the pathogenesis of atherosclerotic plaques and accounts for the high rates of restenosis that occur after percutaneous transluminal coronary angioplasty, a widespread treatment for coronary artery disease. Endothelial lesions trigger intense proliferative signals to the SMCs of the subintima, stimulating their reentry into the cell cycle from a resting G 0 state, resulting in neointima formation and vascular occlusion. Cellular proliferation is negatively controlled by growth-regulatory or tumor-suppressor genes, or both, such as the retinoblastoma gene family members ( RB/p105, p107, RB2…

NeointimaTranscriptional Activationmedicine.medical_specialtyPhysiologyadenovirus; cell cycle; gene therapy; p130; prb2; restenosisCellGenetic VectorsCell Cycle ProteinsPulmonary ArteryMuscle Smooth VascularAdenoviridaeCatheterizationPathogenesisRestenosisRecurrencemedicineAnimalsCarotid StenosisAngioplasty Balloon CoronaryGenes RetinoblastomaCells CulturedNeointimal hyperplasiaWound HealingRetinoblastoma-Like Protein p130business.industryCell growthGenetic transferCell CycleProteinsGenetic TherapyCell cyclemedicine.diseasePhosphoproteinsSurgeryE2F Transcription FactorsRatsDNA-Binding Proteinsmedicine.anatomical_structureCancer researchCardiology and Cardiovascular MedicinebusinessCarotid Artery InjuriesCarrier ProteinsTunica IntimaTranscription Factor DP1Cell DivisionRetinoblastoma-Binding Protein 1Transcription FactorsCirculation research
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Ether-Lipids Are Involved in Retinal Vegf Expression and in Postnatal Hyaloid Vessel Regression

2009

Purpose:Ether-lipids are phospholipids that represent about 13% of retinal lipids and whose exact functions remain unknown. However, the preferential esterification of polyunsaturated fatty acids (PUFAs) at the sn-2 position of ether-lipids and their liberation by an ether-lipid-specific phospholipase A2 suggest their involvement in cell signaling processes. Based on the data showing the persistence of the hyaloid vasculature in ether-lipid-deficient mice (DAPAT-/- mice, Rodemer et al Hum Mol Genet 2003), we further investigated the molecular mechanisms by which ether-lipids may regulate hyaloid vessels regression during post-natal development. Methods:C57BL/6 mice were treated at birth eit…

None C. FourgeuxNone C. JoffreNone L. Bretillonvascular endothelial growth factorNone. Support: None lipids vascular endothelial growth factor developmentC. FourgeuxNone A.M. BronC. JoffreNone B. PasquisCommercial Relationships: N. AcarDevelopmentLipidsC.P. Creuzot-GarcherL. IvingsNone W.W. Just[SDV.AEN] Life Sciences [q-bio]/Food and NutritionA.M. Bron[SDV.MHEP.OS] Life Sciences [q-bio]/Human health and pathology/Sensory OrgansNoneL. BretillonNone C.P. Creuzot-GarcherB. PasquisW.W. JustNone. Support: None lipidsNone L. Ivings
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Estudio del papel de PBX1 como selector terminal de las neuronas dopaminérgicas del bulbo olfatorio

2021

Tesis doctoral 177 p, figuras y tablas.

PBX1diferenciación terminalUNESCO::CIENCIAS DE LA VIDAneuronas dopaminérgicasneurobiologíaselector terminalbulbo olfatorio:CIENCIAS DE LA VIDA [UNESCO]factor de transcripción
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High Lymph Vessel Density and Expression of Lymphatic Growth Factors in Peritoneal Endometriosis

2012

To investigate the occurrence of lymph vessels and lymphangiogenic growth factors in peritoneal lesions, we performed immunohistochemical staining of peritoneal lesions of 37 patients with antibodies against podoplanin (D2-40), lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1), prospero homeobox protein 1 (Prox-1), vascular epithelial growth factor (VEGF)-C/VEGF-D. Overall, 10 lesions were double stained against D2-40 and von Willebrand factor. The lymph vessel density in peritoneal lesion was significantly higher in comparison with healthy peritoneum. All lymph vessel makers could be detected, whereby the lymph vessel density of LYVE-1- and Prox-1-positive lymph vessels was signi…

Pathologychronic inflammatory proceMacrophageVascular Endothelial Growth Factor CVascular Endothelial Growth Factor DVesicular Transport ProteinsFluorescent Antibody TechniquePeritoneal DiseasesAntibodies Monoclonal Murine-Derivedlymphatic disseminationIntercellular Signaling Peptides and ProteinEndometriosiEndothelial CellObstetrics and GynecologyHomeodomain ProteinMiddle AgedImmunohistochemistryLymphangiogenesisLymphatic systemmedicine.anatomical_structureVascular endothelial growth factor CIntercellular Signaling Peptides and ProteinsFemaleLymphEndothelium LymphaticHumanAdultmedicine.medical_specialtyEndometriosisendometriosis; lymphatic dissemination; chronic inflammatory processlymphangiogenesiperitoneal endometriosiLymphatic VesselVesicular Transport ProteinPeritoneummedicineLymphatic vesselLymph node stromal cellHumansLymph sacsLymphatic VesselsHomeodomain ProteinsTumor Suppressor Proteinbusiness.industryMacrophagesTumor Suppressor ProteinsEndothelial CellsBiomarkerchronic inflammatory processPeritoneal DiseasebusinessBiomarkersReproductive Sciences
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Contribution of Anales de Pediatría to the international visibility of Spanish paediatric research in the Web of Science (2010–2014)

2016

Objective: To describe the role of Anales de Pediatría in highlighting Spanish paediatric research, and to identify the journals with which it competes internationally. Material and method: Spanish paediatric articles, including those from Anales de Pediatría were identified using the Paediatrics category of the Science Citation Index (2010–2014), and their volume and document type was analysed. For original articles and review articles, the year, the citation and journal of publication was studied. The journals were classified as general and specialised. The productivity of general journals was analysed according to their language, JCR quartile, and article access. Results: A total of 2701…

Pediatricsmedicine.medical_specialtyBiomedical ResearchInternationalityLibrary scienceBibliometricsPediatricsRJ1-57003 medical and health sciences0302 clinical medicine030225 pediatricsManagement of Technology and InnovationBibliometríaMedicine030212 general & internal medicineCompetitividadPublishingbusiness.industryScientific productionScience Citation IndexProducción científicaFactor de impactoDatabases BibliographicAnales de PediatríaPublishingSpainPeriodicals as TopicbusinessCitationAnales de Pediatría (English Edition)
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Análisis bibliométrico de la producción científica de la Universidad Politécnica de Valencia 1973-2001

2006

Se presenta la proyección de la Universidad Politécnica de Valencia mediante el análisis de su producción científica desde 1973 hasta 2001 inclusive, a partir de los artículos de revista y las comunicaciones a congresos disponibles en las principales bases de datos nacionales e internacionales. Se ha analizado la productividad y distribución temporal, por tipo de documento y por idioma, así como la producción científica por autores y por departamentos, identificando los más productivos. Por otro lado, se ha estudiado la distribución y evolución de la literatura científica, indicando aquellas revistas más utilizadas. Los resultados indican, como aspectos más relevantes, una amplia gama de ár…

Productividadproductivitybibliometric indicatorsAnálisis bibliométricoProducción científicaUNESCO::LINGÜÍSTICA::Lingüística aplicada::DocumentaciónIndicadores bibliométricosFactor de impactoUNESCO::LINGÜÍSTICAlcsh:Zlcsh:Bibliography. Library science. Information resourcesscientific outputBibliography. Library science. Information resources:LINGÜÍSTICA::Lingüística aplicada::Documentación [UNESCO]Bibliometría ; Producción científica ; Indicadores bibliométricos ; Análisis bibliométrico ; Productividad ; Factor de impacto ; Universidad Politécnica de Valencia:LINGÜÍSTICA [UNESCO]bibliometric analysispolytechnic university of valenciaUniversidad Politécnica de ValenciaBibliometríabibliometricsimpact factorZRevista Española de Documentación Científica
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