Search results for "Apoptosis."

showing 10 items of 1794 documents

Synthesis of Combretastatin A-4 and 3′-Aminocombretastatin A-4 derivatives with Aminoacid Containing Pendants and Study of their Interaction with Tub…

2020

Natural product combretastatin A-4 (CA-4) and its nitrogenated analogue 3&prime

Vascular Endothelial Growth Factor ACell cycle checkpoint<i>htert</i>Pharmaceutical ScienceApoptosisAnalytical Chemistrychemistry.chemical_compound0302 clinical medicineDrug DiscoveryStilbenesc-<i>myc</i>Telomerase0303 health sciences<i>vegf</i>biologyNeovascularization PathologicChemistry3′-aminocombretastatin a-4Cell cycle<i>c-Myc</i>VEGFc-MycBiochemistryChemistry (miscellaneous)030220 oncology & carcinogenesisMCF-7 CellsMolecular Medicinecytotoxicitycell cyclehTERTHT29 CellsArticleProto-Oncogene Proteins c-mycmicrotubuleslcsh:QD241-44103 medical and health sciencesStructure-Activity Relationshiplcsh:Organic chemistryMicrotubuleCell Line TumorHumansPhysical and Theoretical Chemistry030304 developmental biologyCell ProliferationCombretastatinCombretastatin A-4Cell growthOrganic ChemistryAntineoplastic Agents PhytogenicTubulintubulinCell cultureA549 Cellsbiology.proteinM Phase Cell Cycle Checkpointscombretastatin a-4Drug Screening Assays AntitumorMolecules
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From the oxygen to the organ protection: Erythropoietin as protagonist in internal medicine

2006

Erythropoietin (EPO), already known as the stimulating hormone for erythropoiesis, has shown different and interesting pleiotropic actions. It does not only affect erythroid cells, but also myeloid cells, lymphocytes and megakaryocytes. This hormone can also enhance phagocytic function of the polymorphonuclear cells and reduce the activation of macrophages, thus modulating the inflammatory process.Moreover, hematopoietic and endothelial cells probably have the same cellular origin, and the discovery of erythropoietin receptors (EPO-R) also on mesangial and myocardial cells, smooth muscle fibrocells and neurons has prompted the study of the non-erythropoietic functions of this hormone.The in…

Vascular Endothelial Growth Factor Amedicine.medical_specialtyIschemiaNeovascularizationIschemiahemic and lymphatic diseasesInternal medicinemedicineErythropoietin (EPO); pleiotropic actions; erythropoietin receptors (EPO-R); VEGFHumansOxygen tensionReceptorHypoxiaErythropoietinPharmacologyClinical Trials as Topicbusiness.industryPleiotropic actionerythropoietin receptors (EPO-R)pleiotropic actionsAngiogenesis Modulating AgentsApoptosiAnemiaShockHematologymedicine.diseaseVEGFHaematopoiesisAngiogenesiEndocrinologyApoptosisErythropoietinErythropoietin (EPO)Erythropoiesismedicine.symptombusinessCardiology and Cardiovascular MedicineHormonemedicine.drugReceptor
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Priming with a combination of proangiogenic growth factors improves wound healing in normoglycemic mice

2011

Growth factors and/or angiogenic factors are supposed to improve wound healing. The aim of our study was to evaluate the effects of subcutaneous pretreatment with combinatory proangiogenic factors on wound closure, mechan - ical properties, vessel density and morphology. Twenty-eight Balb/c mice were divided equally into two groups. A mixture of VEGF (35.0 µg), bFGF (2.5 µg) and P dGF (3.5 µg) was administered subcutaneously 3, 5 and 7 days to 14 mice before full thickness skin punch biopsy wounding, whereas 14 control animals received three injections of 0.2 ml saline solution. Wound sizes were assessed daily and the repaired tissues were harvested 7 days after complete wound closure. Comp…

Vascular Endothelial Growth Factor Amedicine.medical_specialtyPlatelet-derived growth factormedicine.medical_treatmentInjections SubcutaneousUrologyPriming (immunology)Neovascularization PhysiologicArticlechemistry.chemical_compoundMiceSkin Physiological PhenomenaTensile StrengthGeneticsmedicineAnimalsRegenerationSalineSkinPlatelet-Derived Growth FactorMice Inbred BALB CWound HealingOncogeneintegumentary systembusiness.industryGeneral MedicineMolecular medicineSurgeryVascular endothelial growth factor ADrug CombinationsCollagen Type IIIchemistryApoptosisThermographyBlood VesselsAngiogenesis Inducing AgentsFemaleFibroblast Growth Factor 2Wound healingbusiness
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Heart infarct in NOD-SCID mice: therapeutic vasculogenesis by transplantation of human CD34+ cells and low dose CD34+KDR+ cells

2004

Hematopoietic (Hem) and endothelial (End) lineages derive from a common progenitor cell, the hemangioblast: specifically, the human cord blood (CB) CD34+KDR+ cell fraction comprises primitive Hem and End cells, as well as hemangioblasts. In humans, the potential therapeutic role of Hem and End progenitors in ischemic heart disease is subject to intense investigation. Particularly, the contribution of these cells to angiogenesis and cardiomyogenesis in myocardial ischemia is not well established. In our studies, we induced myocardial infarct (MI) in the immunocompromised NOD-SCID mouse model, and monitored the effects of myocardial transplantation of human CB CD34+ cells on cardiac function.…

Vascular Endothelial Growth Factor AneoangiogenesisTime FactorsAngiogenesisCell TransplantationHeart VentriclesCD34Myocardial InfarctionAntigens CD34ApoptosisMice SCIDBiologySCIDPeripheral blood mononuclear cellBiochemistryCulture Media Serum-FreeSerum-FreeCell FusionMiceVasculogenesisMice Inbred NODparasitic diseasesGeneticsAnimalsHumansVentricular Functionendothelial precursorsCell LineageProgenitor cellAntigensMolecular Biologyneoangiogenesis endothelial precursors hematopoietic stem cellsHemodynamicsFetal BloodVascular Endothelial Growth Factor Receptor-2Coculture Techniqueshematopoietic stem cellsCulture MediaTransplantationAutocrine CommunicationCord bloodImmunologycardiovascular systemCancer researchHemangioblastInbred NODCD34neoangiogenesis; endothelial precursors; hematopoietic stem cells; Animals; Antigens CD34; Apoptosis; Autocrine Communication; Cell Fusion; Cell Lineage; Coculture Techniques; Culture Media Serum-Free; Fetal Blood; Heart Ventricles; Hemodynamics; Humans; Mice; Mice Inbred NOD; Mice SCID; Myocardial Infarction; Time Factors; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2; Ventricular Function; Cell Transplantation; Biotechnology; Biochemistry; Molecular Biology; GeneticsBiotechnology
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DNASE1L3 deficiency, new phenotypes, and evidence for a transient type I IFN signaling.

2022

Background: Deoxyribonuclease 1 like 3 (DNASE1L3) is a secreted enzyme that has been shown to digest the extracellular chromatin derived from apoptotic bodies, and DNASE1L3 pathogenic variants have been associated with a lupus phenotype. It is unclear whether interferon signaling is sustained in DNASE1L3 deficiency in humans. Objectives: To explore interferon signaling in DNASE1L3 deficient patients. To depict the characteristic features of DNASE1L3 deficiencies in human. Methods: We identified, characterized, and analyzed five new patients carrying biallelic DNASE1L3 variations. Whole or targeted exome and/or Sanger sequencing was performed to detect pathogenic variations in five juvenile …

VasculitisEndodeoxyribonucleasesImmunologyDNAInflammatory Bowel DiseasesLupus NephritisChromatinANCA Apoptosis DNASE1L3 Interferon-stimulated genes Nucleic acids Systemic lupus erythematosus Type I interferonAntibodies Antineutrophil CytoplasmicSettore MED/38 - Pediatria Generale E SpecialisticaPhenotypeInterferon Type IImmunology and AllergyHumansLupus Erythematosus SystemicInterferonsJournal of clinical immunology
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The Efficacy of Antigen Processing Is Critical for Protection against Cytomegalovirus Disease in the Presence of Viral Immune Evasion Proteins▿

2009

ABSTRACT Cytomegaloviruses (CMVs) code for immunoevasins, glycoproteins that are specifically dedicated to interfere with the presentation of antigenic peptides to CD8 T cells. Nonetheless, the biological outcome is not an immune evasion of the virus, since CD8 T cells can control CMV infection even when immunoevasins are expressed. Here, we compare the processing of a protective and a nonprotective epitope derived from the same viral protein, the antiapoptotic protein M45 in the murine model. The data provide evidence to conclude that protection against CMVs critically depends on antigenic peptides generated in an amount sufficient to exhaust the inhibitory capacity of immunoevasins.

Viral proteinImmunologyAntigen presentationCytomegalovirusBiologyCD8-Positive T-Lymphocytesmedicine.disease_causeMicrobiologyVirusEpitopeEpitopesMiceViral ProteinsImmune systemAntigenVirologyRibonucleotide ReductasesmedicineCytotoxic T cellAnimalsHumansAntigen PresentationAntigen processingVirologyPeptide FragmentsInsect ScienceImmunologyCytomegalovirus InfectionsPathogenesis and ImmunityApoptosis Regulatory Proteins
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Vitamin A Deficiency and Alterations in the Extracellular Matrix

2014

Vitamin A or retinol which is the natural precursor of several biologically active metabolites can be considered the most multifunctional vitamin in mammals. Its deficiency is currently, along with protein malnutrition, the most serious and common nutritional disorder worldwide. It is necessary for normal embryonic development and postnatal tissue homeostasis, and exerts important effects on cell proliferation, differentiation and apoptosis. These actions are produced mainly by regulating the expression of a variety of proteins through transcriptional and non-transcriptional mechanisms. Extracellular matrix proteins are among those whose synthesis is known to be modulated by vitamin A. Reti…

Vitamincollagenkidneyextracellular matrixRetinoic acidlcsh:TX341-641ApoptosisReviewBiologyliverlungExtracellular matrixchemistry.chemical_compoundExtracellularmedicineretinoic acidAnimalsHumansVitamin ATissue homeostasisCell ProliferationNutrition and DieteticsVitamin A DeficiencyRetinolCell Differentiationmedicine.diseasebasement membraneVitamin A deficiencyFibronectinDisease Models AnimalBiochemistrychemistrybiology.proteinlcsh:Nutrition. Foods and food supplyFood ScienceNutrients
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Wee1 inhibition potentiates Wip1-dependent p53-negative tumor cell death during chemotherapy

2016

AbstractInactivation of p53 found in more than half of human cancers is often associated with increased tumor resistance to anti-cancer therapy. We have previously shown that overexpression of the phosphatase Wip1 in p53-negative tumors sensitizes them to chemotherapeutic agents, while protecting normal tissues from the side effects of anti-cancer treatment. In this study, we decided to search for kinases that prevent Wip1-mediated sensitization of cancer cells, thereby interfering with efficacy of genotoxic anti-cancer drugs. To this end, we performed a flow cytometry-based screening in order to identify kinases that regulated the levels of γH2AX, which were used as readout. Another criter…

Wip1ApoptosisCell Cycle ProteinsPharmacologyMESH: G2 Phase Cell Cycle CheckpointsHistonesMESH : PhosphorylationMiceMESH : Cell Cycle ProteinsMESH: AnimalsMESH: Tumor Suppressor Protein p53MESH: HistonesKinaseTp53 mutationsMESH : Mice Transgenic3. Good healthProtein Phosphatase 2CSurvival RateMESH : Antineoplastic AgentsH2ax phosphorylationP53 activationMESH: Protein Phosphatase 2CRNA InterferenceMESH : Colorectal NeoplasmsMESH : Carrier ProteinsHistone H2axMESH: MitochondriaImmunologyHuman fibroblastsMESH: Carrier ProteinsAntineoplastic AgentsMESH: Protein-Tyrosine KinasesMESH: Protein-Serine-Threonine KinasesMESH : Cisplatin03 medical and health sciencesMESH: Cell Cycle ProteinsGenotoxic stressMESH : Protein-Tyrosine KinasesHumansMESH : HistonesAnticancer TherapyMESH: DNA DamageCisplatinMESH: HumansMESH: Phosphorylation[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : HumansMESH : Nuclear Proteins030104 developmental biologyCancer cellMESH: Antineoplastic AgentsCisplatinCarrier ProteinsMESH: Nuclear ProteinsMESH : ApoptosisDna-damage response0301 basic medicineCancer ResearchMESH: Caspase 3MESH : Caspase 3PhosphorylationCytotoxicityMESH : DNA DamageSensitizationmedicine.diagnostic_testCaspase 3Nuclear ProteinsProtein-Tyrosine KinasesMESH : Survival RateMitochondriaG2 Phase Cell Cycle CheckpointsWee1medicine.anatomical_structureMESH : Protein Phosphatase 2COriginal ArticleMESH : MitochondriaColorectal Neoplasmsmedicine.drugMESH : Protein-Serine-Threonine KinasesMESH: Cell Line TumorMESH: Survival RateMESH: Mice TransgenicMESH: RNA InterferencePhosphataseMice Transgenic[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesFlow cytometryCellular and Molecular NeuroscienceCell Line TumorMESH : MicemedicineAnimalsMESH: MiceMESH : Cell Line TumorMESH: ApoptosisCell BiologyMESH : Tumor Suppressor Protein p53MESH: CisplatinCancer researchbiology.proteinMESH : AnimalsMESH : G2 Phase Cell Cycle CheckpointsMESH : RNA InterferenceTumor Suppressor Protein p53MESH: Colorectal NeoplasmsDNA DamageCell Death & Disease
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Depletion ofL-arginine induces autophagy as a cytoprotective response to endoplasmic reticulum stress in human T lymphocytes

2012

PMCID: PMC3494587

X-Box Binding Protein 1Proteasome Endopeptidase ComplexProgrammed cell deathXBP1CD3 ComplexMAP Kinase Signaling SystemRNA SplicingT-LymphocytesT cellDown-RegulationApoptosisRegulatory Factor X Transcription FactorsUbiquitin-Activating EnzymesProtein Serine-Threonine KinasesBiologyArginineLymphocyte ActivationAutophagy-Related Protein 7Jurkat cellsJurkat CellsEndoribonucleasesAutophagymedicineHumansMolecular BiologyCell ProliferationTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCell BiologyBECN1Endoplasmic Reticulum StressG1 Phase Cell Cycle CheckpointsBasic Research Paper3. Good healthCell biologyDNA-Binding Proteinsmedicine.anatomical_structureCytoprotectionApoptosisUnfolded protein responseBeclin-1MitogensApoptosis Regulatory ProteinsLysosomesProto-Oncogene Proteins c-aktTranscription FactorsAutophagy
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Induction of mitochondrial xanthine oxidase activity during apoptosis in the rat mammary gland

2006

Oxidative stress is an important signal for apoptosis to start. So far the mitochondrial respiratory chain has been considered as the major, if not the only, cause of such stress. Here we report that this is not the case. Xanthine oxidase, a O2(-) and H2O2 generating enzyme which is important in causing significant oxidative stress in the cytosol, is also present in the mitochondrial fraction of rat mammary gland. After weaning, during the involution of the mammary gland, massive apoptosis occurs. Mitochondrial xanthine oxidase activity increases and high mitochondrial H2O2 production takes place. Inhibition of xanthine oxidase activity by allopurinol, a specific inhibitor of xanthine oxida…

Xanthine OxidaseAllopurinolRespiratory chainAllopurinolApoptosisWeaningMitochondrionmedicine.disease_causeMitochondrial Proteinschemistry.chemical_compoundMammary Glands AnimalmedicineAnimalsInvolution (medicine)Enzyme InhibitorsXanthine oxidaseChemistryHydrogen PeroxideMitochondriaRatsCell biologyOxidative StressMitochondrial respiratory chainBiochemistryApoptosisOxidative stressmedicine.drugFrontiers in Bioscience
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