Search results for "Transduction"

showing 10 items of 2149 documents

Mitogenic effects of phospholipase D and phosphatidic acid in transiently permeabilized astrocytes: effects of ethanol.

2003

Investigations of lipid-mediated signalling pathways are often limited by a lack of methods for the intracellular delivery of lipid messengers. We established a procedure for the transient permeabilization of astrocytes by an oxygen-insensitive mutant of streptolysin-O (SLO) to investigate the participation of the phospholipase D (PLD) signalling pathway in astroglial cell proliferation. Exogenous PLD, when incubated in the presence of SLO, caused an increase in DNA synthesis (measured by thymidine incorporation) which was completely suppressed by ethanol (0.3%, v/v). In parallel experiments, phosphatidic acid also induced a dose-dependent mitogenic response which, however, was not affected…

Cell Membrane PermeabilityIndolesmedicine.drug_classPhosphatidic AcidsBiologyBiochemistryDiglyceridesCellular and Molecular Neurosciencechemistry.chemical_compoundBacterial ProteinsmedicinePhospholipase DAnimalsEnzyme InhibitorsProtein kinase ACells CulturedDiacylglycerol kinaseDNA synthesisDose-Response Relationship DrugEthanolPhospholipase DPhosphatidic acidDNAProtein kinase inhibitorRatschemistryBiochemistryAstrocytesStreptolysinslipids (amino acids peptides and proteins)Signal transductionMitogensIntracellularCell DivisionSignal TransductionJournal of neurochemistry
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Quinoline-Based Molecules Targeting c-Met, EGF, and VEGF Receptors and the Proteins Involved in Related Carcinogenic Pathways

2020

The quinoline ring system has long been known as a versatile nucleus in the design and synthesis of biologically active compounds. Currently, more than one hundred quinoline compounds have been approved in therapy as antimicrobial, local anaesthetic, antipsychotic, and anticancer drugs. In drug discovery, indeed, over the last few years, an increase in the publication of papers and patents about quinoline derivatives possessing antiproliferative properties has been observed. This trend can be justified by the versatility and accessibility of the quinoline scaffold, from which new derivatives can be easily designed and synthesized. Within the numerous quinoline small molecules developed as a…

Cell SurvivalAngiogenesisPharmaceutical ScienceAntineoplastic AgentsReviewMolecular Dynamics SimulationAnalytical Chemistrylcsh:QD241-441Structure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicinelcsh:Organic chemistryEpidermal growth factorquinolineDrug DiscoverySAR studieHumansPhysical and Theoretical Chemistrycarcinogenic pathwaysProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesantiproliferative compoundChemistryDrug discoveryOrganic ChemistryQuinolineBiological activityProto-Oncogene Proteins c-metantiproliferative compoundstargeted therapySettore CHIM/08 - Chimica FarmaceuticaSmall moleculeErbB Receptorscarcinogenic pathwayReceptors Vascular Endothelial Growth FactorSAR studiesChemistry (miscellaneous)030220 oncology & carcinogenesisQuinolinesCancer researchMolecular Medicinekinases modulatorkinases modulatorsbiological dataSignal TransductionMolecules
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IgG1 B cell receptor signaling is inhibited by CD22 and promotes the development of B cells whose survival is less dependent on Ig alpha/beta.

2007

We describe a mouse strain in which B cell development relies either on the expression of membrane-bound immunoglobulin (Ig) gamma1 or mu heavy chains. Progenitor cells expressing gamma1 chains from the beginning generate a peripheral B cell compartment of normal size with all subsets, but a partial block is seen at the pro- to pre-B cell transition. Accordingly, gamma1-driven B cell development is disfavored in competition with developing B cells expressing a wild-type (WT) IgH locus. However, the mutant B cells display a long half-life and accumulate in the mature B cell compartment, and even though partial truncation of the Ig alpha cytoplasmic tail compromises their development, it does…

Cell SurvivalCellular differentiationSialic Acid Binding Ig-like Lectin 2ImmunologyNaive B cellB-cell receptorImmunoglobulinsReceptors Antigen B-CellBiologyArticle03 medical and health sciencesMice0302 clinical medicinemedicineImmunology and AllergyAnimalsProgenitor cellMemory B cellB cell030304 developmental biologyCell ProliferationMice Knockout0303 health sciencesB-LymphocytesCell growthCD22Toll-Like ReceptorsCell DifferentiationArticlesMolecular biologyCell biologyMice Inbred C57BLmedicine.anatomical_structureImmunoglobulin GMutationCalciumDimerizationCD79 AntigensSpleen030215 immunologyProtein BindingSignal TransductionThe Journal of experimental medicine
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Colon Cancer Stem Cells: Promise of Targeted Therapy

2010

First developed for hematologic disorders, the concept of cancer stem cells (CSCs) was expanded to solid tumors, including colorectal cancer (CRC). The traditional model of colon carcinogenesis includes several steps that occur via mutational activation of oncogenes and inactivation of tumor suppressor genes. Intestinal epithelial cells exist for a shorter amount of time than that required to accumulate tumor-inducing genetic changes, so researchers have investigated the concept that CRC arises from the long-lived stem cells, rather than from the differentiated epithelial cells. Colon CSCs were originally identified through the expression of the CD133 glycoprotein using an antibody directed…

Cell SurvivalColonColorectal cancermedicine.medical_treatmentMetastasisTargeted therapyColon cancer stem cellsCancer stem cellBiomarkers TumormedicineAnimalsHumansHepatologybiologyCD44GastroenterologyLGR5Cell Differentiationmedicine.diseaseGene Expression Regulation NeoplasticCell Transformation NeoplasticDrug Resistance NeoplasmColonic NeoplasmsNeoplastic Stem CellsCancer researchbiology.proteinStem cellSignal TransductionAdult stem cell
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NKG2D induces Mcl-1 expression and mediates survival of CD8 memory T cell precursors via phosphatidylinositol 3-kinase.

2013

Abstract Memory formation of activated CD8 T cells is the result of a specific combination of signals that promote long-term survival and inhibit differentiation into effector cells. Much is known about initial cues that drive memory formation, but it is poorly understood which signals are essential during the intermediate stages before terminal differentiation. NKG2D is an activating coreceptor on Ag-experienced CD8 T cells that promotes effector cell functions. Its role in memory formation is currently unknown. In this study, we show that NKG2D controls formation of CD8 memory T cells by promoting survival of precursor cells. We demonstrate that NKG2D enhances IL-15–mediated PI3K signalin…

Cell SurvivalImmunologyCytomegalovirusBiologyCD8-Positive T-LymphocytesLymphocyte ActivationMiceMemory cellPrecursor cellmedicineImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorReceptors ImmunologicInterleukin-15Mice KnockoutPrecursor Cells T-LymphoidNK cells; NKG2D; CD8 T cellsEffectorCell DifferentiationNKG2DNKG2D; CD8 T cell memory; Mcl1; PI3KCell biologyMice Inbred C57BLmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2NK Cell Lectin-Like Receptor Subfamily KCytomegalovirus InfectionsMyeloid Cell Leukemia Sequence 1 ProteinPhosphatidylinositol 3-KinaseMemory T cellImmunologic MemoryCD8Signal TransductionJournal of immunology (Baltimore, Md. : 1950)
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Geldanamycin-induced osteosarcoma cell death is associated with hyperacetylation and loss of mitochondrial pool of heat shock protein 60 (hsp60)

2013

Osteosarcoma is one of the most malignant tumors of childhood and adolescence that is often resistant to standard chemo- and radio-therapy. Geldanamycin and geldanamycin analogs have been recently studied as potential anticancer agents for osteosarcoma treatment. Here, for the first time, we have presented novel anticancer mechanisms of geldanamycin biological activity. Moreover, we demonstrated an association between the effects of geldanamycin on the major heat shock proteins (HSPs) and the overall survival of highly metastatic human osteosarcoma 143B cells. We demonstrated that the treatment of 143B cells with geldanamycin caused a subsequent upregulation of cytoplasmic Hsp90 and Hsp70 w…

Cell SurvivalLactams Macrocycliclcsh:MedicineApoptosisBone NeoplasmsBiologyMitochondrionMitochondrial Proteinschemistry.chemical_compoundGeldanamycin Hsp60 Osteosarcoma cellHeat shock proteinCell Line Tumorpolycyclic compoundsBenzoquinonesHumansHeat shocklcsh:ScienceCell ProliferationOsteosarcomaMultidisciplinaryAntibiotics Antineoplasticlcsh:RAcetylationChaperonin 60GeldanamycinHsp90Molecular biologyMitochondriaProtein TransportchemistryCancer cellCancer researchbiology.proteinApoptotic signaling pathwayHSP60lcsh:QDrug Screening Assays AntitumorProtein Processing Post-TranslationalResearch ArticleSignal Transduction
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The role of signal transducers and activators of transcription in T inflammatory bowel diseases.

2003

Signal transducers and activators of transcription (STAT) proteins are intracellular effector molecules of cytokine-modulated signaling. On the one hand, they play an important role in hematopoiesis and the development of the human immune system. STAT transcription factors are necessary for embryogenesis and the maintenance of the mammalian immune response. In the adult, STAT signaling is responsible for T-cell polarization toward interferon gamma-secreting Th1 T cells or interleukin 4-producing Th2 cells. On the other hand, these proteins are involved in the regulation of T-cell survival. STAT activation is strongly associated with tyrosine phosphorylation by tyrosine kinases, namely Jak1,…

Cell SurvivalT-LymphocytesGastroenterologyTyrosine phosphorylationBiologyInflammatory Bowel DiseasesstatCell biologyHematopoiesischemistry.chemical_compoundchemistryInterferonImmunologySTAT proteinmedicineTrans-ActivatorsImmunology and AllergyHumansProtein inhibitor of activated STATSignal transductionSTAT4STAT6medicine.drugSignal TransductionInflammatory bowel diseases
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Cytolethal distending toxin (CDT): a bacterial weapon to control host cell proliferation ?

2001

Cytolethal distending toxins (CDT) constitute a family of genetically related bacterial protein toxins able to stop the proliferation of numerous cell lines. This effect is due to their ability to trigger in target cells a signaling pathway that normally prevents the transition between the G2 and the M phase of the cell cycle. Produced by several unrelated Gram-negative mucosa-associated bacterial species, CDTs are determined by a cluster of three adjacent genes (cdtA, cdtB, cdtC) encoding proteins whose respective role is not yet fully elucidated. The CDT-B protein presents sequence homology to several mammalian and bacterial phosphodiesterases, such as DNase I. The putative nuclease activ…

Cell cycle checkpointCell divisionCytolethal distending toxinCell growthBacterial ToxinsCell cycleG2-M DNA damage checkpointBiologyMicrobiologyMicrobiologyCell biologyCell Line[SDV.MP]Life Sciences [q-bio]/Microbiology and ParasitologyGram-Negative BacteriaGeneticsAnimalsHumansSignal transductionGram-Negative Bacterial InfectionsMolecular BiologyGene[SDV.MP] Life Sciences [q-bio]/Microbiology and ParasitologyCell Division
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Modulation of Cell Cycle Components by Epigenetic and Genetic Events

2005

Cell cycle progression is monitored by surveillance mechanisms, or cell cycle checkpoints, that ensure that initiation of a later event is coupled with the completion of an early cell cycle event. Deregulated proliferation is a characteristic feature of tumor cells. Moreover, defects in many of the molecules that regulate the cell cycle have been implicated in cancer formation and progression. Key among these are p53, the retinoblastoma protein (pRb) and its related proteins, p107 and pRb2/p130, and cdk inhibitors (p15, p16, p18, p19, p21, p27), all of which act to keep the cell cycle from progressing until all repairs to damaged DNA have been completed. The pRb (pRb/p16(INK4a)/cyclin D1) a…

Cell cycle checkpointCyclin ABiologymedicine.disease_causeModels BiologicalRetinoblastoma ProteinEpigenesis GeneticCyclin-dependent kinaseNeoplasmsmedicineAnimalsHumansEpigeneticsCell ProliferationCell growthCell CycleRetinoblastoma proteinHematologyCell cycleCell biologyOncologyDisease Progressionbiology.proteinTumor Suppressor Protein p53biological phenomena cell phenomena and immunityCarcinogenesisSignal TransductionSeminars in Oncology
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Cell cycle arrest and induction of apoptosis by cajanin stilbene acid from Cajanus cajan in breast cancer cells

2015

Abstract Background: The low abundant cajanin stilbene acid (CSA) from Pigeon Pea ( Cajanus cajan ) has been shown to kill estrogen receptor α positive cancer cells in vitro and in vivo . Downstream effects such as cell cycle and apoptosis-related mechanisms have not been analyzed yet. Material and methods: We analyzed the activity of CSA by means of flow cytometry (cell cycle distribution, mitochondrial membrane potential, MMP), confocal laser scanning microscopy (MMP), DNA fragmentation assay (apoptosis), Western blotting (Bax and Bcl-2 expression, caspase-3 activation) as well as mRNA microarray hybridization and Ingenuity pathway analysis. Results: CSA induced G2/M arrest and apoptosis …

Cell cycle checkpointDNA damageCellPharmaceutical ScienceApoptosisBiologyFlow cytometryCajanusStilbenesDrug DiscoverymedicineHumansbcl-2-Associated X ProteinMembrane Potential MitochondrialPharmacologymedicine.diagnostic_testCaspase 3Cell Cycle CheckpointsCell cycleMolecular biologySalicylatesGene Expression Regulation Neoplasticmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2Complementary and alternative medicineApoptosisCancer cellMCF-7 CellsMolecular MedicineDNA fragmentationDNA DamageSignal TransductionPhytomedicine
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