Search results for "Signal"

showing 10 items of 6924 documents

A helicopter perspective on TB biomarkers: pathway and process based analysis of gene expression data provides new insight into TB pathogenesis.

2013

Biomarker host genetic signatures are considered key tools for improved early diagnosis of tuberculosis (TB) disease (development). The analysis of gene expression changes based on a limited number of genes or single study designs, however, may not be sufficient for the identification of universal diagnostic biomarker profiles. Here we propose that biological pathway and process based analyses from multiple data sets may be more relevant for identification of key pathways in TB pathogenesis, and may reveal novel candidate diagnostic TB biomarkers. A number of independent genome-wide gene expression studies have recently been performed to study expression of biomarkers for TB disease. We hav…

Tuberculosislcsh:MedicineDiseaseBioinformaticsMycobacterium tuberculosisBiological pathway03 medical and health sciences0302 clinical medicineGene expressionmedicineHumansTuberculosislcsh:ScienceGene030304 developmental biology0303 health sciencesMultidisciplinarybiologyGene Expression Profilinglcsh:Rbiology.organism_classificationmedicine.disease3. Good healthGene expression profiling030220 oncology & carcinogenesisBiomarker (medicine)lcsh:QBiomarkersResearch ArticleSignal TransductionPLoS ONE
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Acidic Environment Leads to ROS-Induced MAPK Signaling in Cancer Cells

2011

Tumor micromilieu often shows pronounced acidosis forcing cells to adapt their phenotype towards enhanced tumorigenesis induced by altered cellular signalling and transcriptional regulation. In the presents study mechanisms and potential consequences of the crosstalk between extra- and intracellular pH (pH(e), pH(i)) and mitogen-activated-protein-kinases (ERK1/2, p38) was analyzed. Data were obtained mainly in AT1 R-3327 prostate carcinoma cells, but the principle importance was confirmed in 5 other cell types. Extracellular acidosis leads to a rapid and sustained decrease of pH(i) in parallel to p38 phosphorylation in all cell types and to ERK1/2 phosphorylation in 3 of 6 cell types. Furth…

Tumor PhysiologyIntracellular Spacelcsh:MedicineSignal transductionERK signaling cascadeMolecular cell biologyNeoplasmsBasic Cancer ResearchTumor MicroenvironmentSignaling in Cellular ProcessesPhosphorylationCyclic AMP Response Element-Binding ProteinCreb Signalinglcsh:ScienceCellular Stress ResponsesMultidisciplinaryKinaseMechanisms of Signal TransductionSignaling cascadesHydrogen-Ion ConcentrationProtein-Tyrosine KinasesCell biologyOncologyMedicinePhosphorylationMitogen-Activated Protein KinasesSodium-Potassium-Exchanging ATPaseIntracellularResearch ArticleCell SurvivalMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesIntracellular pHBiologyCREBModels BiologicalCell GrowthDogsCell Line TumorAnimalsHumansProtein Kinase InhibitorsBiologyPI3K/AKT/mTOR pathwaylcsh:RRatsEnzyme ActivationCancer cellbiology.proteinlcsh:QExtracellular SpaceReactive Oxygen SpeciesAcidsPLoS ONE
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Binding of PTEN to specific PDZ domains contributes to PTEN protein stability and phosphorylation by microtubule-associated serine/threonine kinases

2005

The tumor suppressor phosphatase PTEN is a key regulator of cell growth and apoptosis that interacts with PDZ domains from regulatory proteins, including MAGI-1/2/3, hDlg, and MAST205. Here we identified novel PTEN-binding PDZ domains within the MAST205-related proteins, syntrophin-associated serine/threonine kinase and MAST3, characterized the regions of PTEN involved in its interaction with distinctive PDZ domains, and analyzed the functional consequences on PTEN of PDZ domain binding. Using a panel of PTEN mutations, as well as PTEN chimeras containing distinct domains of the related protein TPTE, we found that the PTP and C2 domains of PTEN do not affect PDZ domain binding and that the …

Tumor Suppressor Proteins/chemistry/ metabolismTime FactorsAmino Acid MotifsPlasma protein bindingBiochemistryMicrotubulesSerineDiscs Large Homolog 1 ProteinProtein structureSaccharomyces cerevisiae/metabolismPhosphorylationGlutathione Transferaseddc:616Nucleoside-Phosphate Kinase/metabolismbiologyChemistryDystrophin-Associated Proteins/ chemistrySignal transducing adaptor proteinProtein-Serine-Threonine Kinases/metabolismRecombinant Fusion Proteins/chemistryGuanylate KinaseCell biologyCOS CellsMicrotubule-Associated Proteins/metabolismPhosphorylationProteins/metabolismGlutathione Transferase/metabolismMicrotubule-Associated ProteinsMicrotubules/ metabolismPlasmidsProtein BindingCèl·lulesRecombinant Fusion ProteinsPDZ domainSaccharomyces cerevisiaeProtein Serine-Threonine KinasesTransfectionModels BiologicalTwo-Hybrid System TechniquesDiscs Large Homolog 1 ProteinPTENAnimalsHumansImmunoprecipitationProteïnes supressores de tumorsMolecular BiologyAdaptor Proteins Signal TransducingTumor Suppressor ProteinsPTEN PhosphohydrolaseProteinsMembrane ProteinsCell BiologyPlasmids/metabolismPhosphoric Monoester HydrolasesProtein Structure TertiaryDystrophin-Associated ProteinsMutationCancer researchbiology.proteinNucleoside-Phosphate KinaseCarrier ProteinsGuanylate KinasesPhosphoric Monoester Hydrolases/chemistry/ metabolism
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Dissecting signaling and functions of adhesion G protein-coupled receptors

2012

G protein-coupled receptors (GPCRs) comprise an expanded superfamily of receptors in the human genome. Adhesion class G protein-coupled receptors (adhesion-GPCRs) form the second largest class of GPCRs. Despite the abundance, size, molecular structure, and functions in facilitating cell and matrix contacts in a variety of organ systems, adhesion-GPCRs are by far the most poorly understood GPCR class. Adhesion-GPCRs possess a unique molecular structure, with extended N-termini containing various adhesion domains. In addition, many adhesion-GPCRs are autoproteolytically cleaved into an N-terminal fragment (NTF, NT, α-subunit) and C-terminal fragment (CTF, CT, β-subunit) at a conserved GPCR au…

Tumor biologyGeneral NeuroscienceAdhesionComputational biologyBiologyGeneral Biochemistry Genetics and Molecular BiologyCell biologyGPR56History and Philosophy of ScienceHuman genomeSignal transductionCell adhesionReceptorhormones hormone substitutes and hormone antagonistsG protein-coupled receptorAnnals of the New York Academy of Sciences
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Transmission of Information in Neoplasia by Extracellular Vesicles.

2015

Paracrine interactions among neoplastic and nonneoplastic cells in the immediate tumor microenvironment are important for tumor growth and metastatic spreading. Most of the studies in the past decade addressing these cellular interactions have focused on tumor cell-derived soluble molecules. Recently, these studies and interest have shifted to nanosized extracellular vesicles (EVs) and especially ectosome and exosome-associated molecules [1]. They contain not only proteins, but also lipids, mRNA, and microRNA [1], which can regulate gene expression in their target cells in a much more pleiotropic manner [1]. While exosomes originate by a sequential process of inward budding of late endosome…

Tumor microenvironmentCell signalingStromal cellGeneral Immunology and MicrobiologyArticle SubjectEndosomeCellular differentiationlcsh:RParacrine Communicationlcsh:MedicineGeneral MedicineCell CommunicationBiologyExosomesGeneral Biochemistry Genetics and Molecular BiologyMicrovesiclesCell biologyParacrine signallingExtracellular VesiclesEditorialNeoplasmsParacrine CommunicationHumansBioMed research international
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Hematologic malignancies: The exosome contribution in tumor progression

2020

Abstract The bone marrow, composed of cells, extracellular matrix, and soluble factors, such as cytokines, chemokines and signaling molecules, provides a favorable microenvironment for hematologic tumor progression and for the development of drug resistance. Recently, extracellular vesicles (EVs), released by tumor and surrounding cells, have emerged as important players within the bone marrow niche. Here we will discuss the current knowledge on the EV- mediated crosstalk between tumor and normal cells, in order to better understand how vesicles can contribute to tumor progression. Advances in the knowledge of the role of cell-derived EVs in tumor microenvironment highlight the possibility …

Tumor microenvironmentChemokineCell signalingbiologybusiness.industryExosomeMicrovesiclesExtracellular matrixmedicine.anatomical_structureTumor progressionCancer researchbiology.proteinMedicineBone marrowbusiness
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Targeting cancer stem cells and the tumor microenvironment

2015

Compelling evidence indicates that the survival and behavior of cancer stem cells (CSCs) are positively regulated by specific stimuli received from the tumor microenvironment, which dictates the maintenance of stemness, invasiveness, and protection against drug-induced apoptotic signals. CSCs are per se endowed with multiple treatment resistance capabilities, thus the eradication of CSC pools offers a precious strategy in achieving a long-term cancer remission. Numerous therapies, aimed at eradicating CSCs, have been elaborated such as: (i) selective targeting of CSCs, (ii) modulating their stemness and (iii) influencing the microenvironment. In this context, markers commonly exploited to i…

Tumor microenvironmentCyclopamineCancer therapymedicine.medical_treatmentCellular differentiationCancer stem cellWnt signaling pathwayContext (language use)BiologyStemness modulator drugCXCR4Targeted therapyTargeted therapychemistry.chemical_compoundchemistryTumor microenvironmentCancer stem cellmedicineCancer research
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Progression of colorectal cancers correlates with overexpression and loss of polarization of expression of the htid-1 tumor suppressor.

2007

Recently, we identified htid-1, the human counterpart of the Drosophila tumor suppressor gene lethal(2)tumorous imaginal discs [l(2)tid], as a direct molecular ligand of the adenomatous polyposis coli (APC) tumor suppressor. The gene encodes three cytosolic (Tid50, Tid48 and Tid46) and three mitochondrial (Tid43, Tid40 and Tid38) proteins. In the colorectal epithelium the cytosolic forms hTid50/hTid48 interact under physiological conditions with the N-terminal region of APC. This complex which associates with additional proteins such as Hsp70, Hsc70, Actin, Dvl and Axin defines a novel physiological state of APC unrelated to beta-catenin degradation. Here we show that the expression of the …

Tumor suppressor geneProtein familyAdenomatous polyposis coliColorectal cancerAntibodies NeoplasmRNA SplicingAdenomatous Polyposis Coli ProteinGeneticsmedicineHumansHSP70 Heat-Shock ProteinsRNA NeoplasmIntestinal MucosaDNA PrimersGeneticsOncogenebiologyTumor Suppressor ProteinsWnt signaling pathwayCell DifferentiationGeneral MedicineCell cycleHSP40 Heat-Shock Proteinsmedicine.diseaseGene Expression Regulation NeoplasticChaperone (protein)biology.proteinCancer researchDisease ProgressionColorectal NeoplasmsInternational journal of molecular medicine
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The tumor suppressor CYLD controls the function of murine regulatory T cells.

2012

Abstract CYLD was originally identified as a tumor suppressor gene mutated in familial cylindromatosis, an autosomal dominant predisposition to multiple benign neoplasms of the skin known as cylindromas. The CYLD protein is a deubiquitinating enzyme that acts as a negative regulator of NF-κB and JNK signaling through its interaction with NEMO and TNFR-associated factor 2. We have previously described a novel mouse strain that expresses solely and excessively a naturally occurring splice variant of CYLD (CYLDex7/8). In this study, we demonstrate that CYLD plays a critical role in Treg development and function. T cells of CYLDex7/8 mice had a hyperactive phenotype manifested by increased prod…

Tumor suppressor geneT cellImmunologyBiologyT-Lymphocytes RegulatoryDeubiquitinating Enzyme CYLDlaw.inventionProinflammatory cytokineMicelawmedicineImmunology and AllergyAnimalsCTLA-4 AntigenIL-2 receptorTumor Suppressor ProteinsInterleukin-2 Receptor alpha SubunitIntracellular Signaling Peptides and ProteinsNF-kappa BFOXP3PhenotypeMice Mutant StrainsCell biologyDeubiquitinating Enzyme CYLDCysteine Endopeptidasesmedicine.anatomical_structureGene Expression RegulationImmunologySuppressorJournal of immunology (Baltimore, Md. : 1950)
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Naturally occurring short splice variant of CYLD positively regulates dendritic cell function

2009

Abstract Deubiquitination of NF-κB members by CYLD is crucial in controlling the magnitude and nature of cell activation. The role of the naturally occurring CYLD splice variant in dendritic cell (DC) function was analyzed using CYLDex7/8 mice, which lack the full-length CYLD (flCYLD) transcript and overexpress the short splice variant (sCYLD). Bone marrow–derived DCs from CYLDex7/8 mice display a hyperactive phenotype in vitro and in vivo and have a defect in establishing tolerance with the use of DEC-205–mediated antigen targeting to resting DCs. The combination of sCYLD overexpression and lack of flCYLD in CYLDex7/8 DCs leads to enhanced NF-κB activity accompanied by an increased nuclear…

Tumor suppressor geneTransgeneImmunologyRegulatorMice TransgenicBiologyBiochemistryDeubiquitinating Enzyme CYLDMiceAnimalsAntigen-presenting cellNF-kappa BDendritic CellsCell BiologyHematologyDendritic cellDeubiquitinating Enzyme CYLDCell biologyMice Inbred C57BLAlternative SplicingCysteine EndopeptidasesPhenotypeImmunologySignal transductionCell activationSignal TransductionBlood
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