Search results for "signal transduction."

showing 10 items of 1278 documents

Prognostic significance of Focal Adhesion Kinase (FAK) in node-negative breast cancer.

2015

552 Background: Focal adhesion kinase (FAK) is a cytoplasmic tyrosine kinase playing an important role as a key mediator for signal transduction. We examined the subtype specific prognostic signifi...

CYTOPLASMIC TYROSINE KINASECancer ResearchPathologymedicine.medical_specialtybusiness.industrymedicine.diseaseNode negativeFocal adhesionMediatorBreast cancerOncologymedicineCancer researchSignal transductionbusinessJournal of Clinical Oncology
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Muscle repair after physiological damage relies on nuclear migration for cellular reconstruction

2021

Muscle repair without stem cells Skeletal muscle is a mechanical organ that endures cellular damage after contraction. Lesions caused by external injury can be repaired by muscle stem cells, which fuse with injured cells or create entirely new myofibers. Roman et al . describe a cell-autonomous repair process that is independent of muscle stem cells (see the Perspective by McNally and Demonbreun). After localized damage, myonuclei migrate to injury sites and locally deliver messenger RNA for cellular reconstruction. This myofiber self-repair represents a model for understanding the restoration of muscle architecture in health and disease. —BAP

Calcium metabolismMultidisciplinaryChemistryRegeneration (biology)Skeletal muscleCell biologymedicine.anatomical_structuremedicineStem cellmedicine.symptomNuclear migrationSignal transductionProcess (anatomy)Muscle contractionscience
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CaMKII inhibition reduces electrical activation heterogeneities caused by mechanical stretch in the myocardium

2020

Abstract Introduction Ca2+/calmodulin-dependant protein kinase II (CaMKII) activity in cardiomyocytes plays a crucial role in their contractility. Increased CaMKII signalling has been associated with mechanical stretch, often caused in the border zone of myocardial infarction. CaMKII upregulation causes a mishandling of intracellular calcium, a precursor of multiple pro-arrhythmic mechanisms, such as early afterdepolarisations. Purpose In this study, we aim to quantify the effects of KN-93 -a CaMKII inhibitor- on wave dynamics, in order to investigate its effectiveness as an anti-arrhythmic agent. Methods An isolated Langendorff model was constructed based on rabbit hearts (n=18) and poster…

Calmodulinbiologybusiness.industrychemistry.chemical_elementCardiac arrhythmiaTorsades de pointesCalciumPharmacologymedicine.diseasechemistryCa2+/calmodulin-dependent protein kinaseHeart failurebiology.proteinmedicineSignal transductionCardiology and Cardiovascular MedicinebusinessAnti-Arrhythmia AgentsEuropean Heart Journal
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Novel pathway in Bcr-Abl signal transduction involves Akt-independent, PLC-γ1-driven activation of mTOR/p70S6-kinase pathway

2009

In chronic myeloid leukemia, activation of the phosphoinositide 3-kinase (PI3K)/Akt pathway is crucial for survival and proliferation of leukemic cells. Essential downstream molecules involve mammalian target of rapamycin (mTOR) and S6-kinase. Here, we present a comprehensive analysis of the molecular events involved in activation of these key signaling pathways. We provide evidence for a previously unrecognized phospholipase C-gamma1 (PLC-gamma1)-controlled mechanism of mTOR/p70S6-kinase activation, which operates in parallel to the classical Akt-dependent machinery. Short-term imatinib treatment of Bcr-Abl-positive cells caused dephosphorylation of p70S6-K and S6-protein without inactivat…

Cancer ResearchBlotting WesternMedizinFusion Proteins bcr-ablApoptosisProtein Serine-Threonine KinasesBiologyPiperazinesMiceLeukemia Myelogenous Chronic BCR-ABL Positivehemic and lymphatic diseasesGeneticsAnimalsHumansRNA Small InterferingProtein Kinase InhibitorsMolecular BiologyProtein kinase BCAMKPI3K/AKT/mTOR pathwayPhospholipase C gammaCell growthKinaseTOR Serine-Threonine KinasesRPTORIntracellular Signaling Peptides and ProteinsRibosomal Protein S6 Kinases 70-kDaCell biologyEnzyme ActivationPyrimidinesBenzamidesembryonic structuresImatinib MesylateCancer researchPhosphorylationSignal transductionProto-Oncogene Proteins c-aktSignal TransductionOncogene
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Differences in the mechanisms of growth control in contact-inhibited and serum-deprived human fibroblasts

1997

In the present work we studied mechanisms of growth control in contact-inhibited and serum-deprived human diploid fibroblasts. The observation that the effects on [3H]thymidine incorporation and reduction of retinoblastoma gene product-phosphorylation were additive when contact-inhibition and serum-deprivation were combined led us to the conclusion that the underlying mechanisms might be different. Both contact-inhibition and serum-deprivation led to a strong decrease of cdk4-kinase-activity and cdk2-phosphorylation at Thr 160, while the total amounts of cdk4 and cdk2 remained constant. In contact-inhibited cells, we revealed a strong protein accumulation of the cdk2-inhibitor p27 and a sli…

Cancer ResearchCell Cycle ProteinsProtein Serine-Threonine KinasesRetinoblastoma ProteinCulture Media Serum-FreeS PhaseCyclin D1CyclinsProto-Oncogene ProteinsCDC2-CDC28 KinasesGeneticsmedicineHumansCyclin D1Cyclin D3PhosphorylationCyclin D3FibroblastMolecular BiologyCyclin-Dependent Kinase Inhibitor p16CyclinbiologyCell growthTumor Suppressor ProteinsCyclin-Dependent Kinase 2Cyclin-dependent kinase 2G1 PhaseCyclin-Dependent Kinase 4FibroblastsDiploidyCyclin-Dependent KinasesCulture MediaCell biologymedicine.anatomical_structureCell culturebiology.proteinbiological phenomena cell phenomena and immunitySignal transductionMicrotubule-Associated ProteinsCell DivisionCyclin-Dependent Kinase Inhibitor p27Oncogene
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P11.09 Pan-RTK inhibition of sLRIG1 mediates AXL downregulation in Glioblastoma

2019

Abstract INTRODUCTION Aberrant regulation of receptor tyrosine kinase (RTK) activity is characteristic of Glioblastoma (GBM). However, RTK-based targeted therapies have been largely unsuccessful in GBM patients, partially due to the complexity and redundance of RTK signaling. LRIG1 (Leucine-rich Repeats and ImmunoGlobulindomains protein 1) is known as an endogenous inhibitor of epidermal growth factor receptor (EGFR) during health and disease, however its mechanism of action is poorly understood. We previously showed that the soluble form of LRIG1 potently inhibits of GBM growth in vivo, irrespective of EGFR expression level and status, suggesting the involvement of other RTKs. Here, we aim…

Cancer ResearchCell growthChemistrymedicine.diseasePoster PresentationsOncologyDownregulation and upregulationmedicineCancer researchNeurology (clinical)Cellular MorphologyTransluminal attenuation gradientSignal transductionGlioblastoma
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Mitochondrial chaperones in cancer: From molecular biology to clinical diagnostics

2006

Mitochondria are cell organelles involved in processes of cell life and death, and therefore also in tumoral transformation. Indeed, mitochondria dysfunction is a prominent feature of cancer cells. Mitochondrial proteins and DNA have also been previously studied as markers of tumorigenesis. Heat shock proteins (HSPs) are ubiquitous evolutionary conserved proteins. HSPs enhance their expression in stressed cells and they are involved in gene expression regulation, DNA replication, signal transduction, differentiation, apoptosis, cellular senescence or immortalization. This review reflects recent views on the role of some mitochondrial molecular chaperones as prohibitin, mortalin and HSP60/HS…

Cancer ResearchCellBiologyMitochondrionmedicine.disease_causeMitochondrial ProteinsNeoplasmsHeat shock proteinmedicineHumanscancerProhibitinHeat-Shock ProteinsPharmacologyMolecular biologyMitochondriaCell biologyCell Transformation Neoplasticmedicine.anatomical_structureOncologyCancer cellMolecular MedicineHSP60Signal transductionCarcinogenesisMolecular ChaperonesCancer Biology & Therapy
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IL1β Induces Mesenchymal Stem Cells Migration and Leucocyte Chemotaxis Through NF-κB

2012

Mesenchymal stem cells are often transplanted into inflammatory environments where they are able to survive and modulate host immune responses through a poorly understood mechanism. In this paper we analyzed the responses of MSC to IL-1β: a representative inflammatory mediator. Microarray analysis of MSC treated with IL-1β revealed that this cytokine activateds a set of genes related to biological processes such as cell survival, cell migration, cell adhesion, chemokine production, induction of angiogenesis and modulation of the immune response. Further more detailed analysis by real-time PCR and functional assays revealed that IL-1β mainly increaseds the production of chemokines such as CC…

Cancer ResearchChemokineMigration and adhesionmedicine.medical_treatmentInterleukin-1betaBiologyArticleInterleukin 1βExtracellular matrixCell MovementCell AdhesionLeukocytesmedicineHumansCell adhesionCell ProliferationOligonucleotide Array Sequence AnalysisCell adhesion moleculeGene Expression ProfilingChemotaxisNF-kappa BMesenchymal Stem CellsCell migrationCell BiologyFibronectinsI-kappa B KinaseCell biologyChemotaxis LeukocyteHEK293 CellsCXCL3CytokineGene Knockdown Techniquesbiology.proteinIntercellular Signaling Peptides and ProteinsRNA InterferenceCollagenLamininChemokinesInflammation MediatorsStem cellSignal TransductionDevelopmental BiologyStem Cell Reviews and Reports
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Moguntinones--new selective inhibitors for the treatment of human colorectal cancer.

2014

Abstract 3-Indolyl and 3-azaindolyl-4-aryl maleimide derivatives, called moguntinones (MOG), have been selected for their ability to inhibit protein kinases associated with angiogenesis and induce apoptosis. Here, we characterize their mode of action and their potential clinical value in human colorectal cancer in vitro and in vivo. MOG-19 and MOG-13 were characterized in vitro using kinase, viability, and apoptosis assays in different human colon cancer (HT-29, HCT-116, Caco-2, and SW480) and normal colon cell lines (CCD-18Co, FHC, and HCoEpiC) alone or in combination with topoisomerase I inhibitors. Intracellular signaling pathways were analyzed by Western blotting. To determine their pot…

Cancer ResearchIndolesColorectal cancerAngiogenesisApoptosisBiologyPharmacologyMetastasisMaleimidesMiceIn vivomedicineAnimalsHumansPI3K/AKT/mTOR pathwayKinaseTOR Serine-Threonine Kinasesmedicine.diseaseXenograft Model Antitumor AssaysOncologyApoptosisSignal transductionCaco-2 CellsTopoisomerase I InhibitorsColorectal NeoplasmsHT29 CellsProto-Oncogene Proteins c-aktSignal TransductionMolecular cancer therapeutics
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Novel insulin receptor substrate 1 and 2 variants in breast and colorectal cancer

2013

The insulin/insulin-like growth factor pathway is involved in breast and colorectal cancer (CRC) development. In the present study, we analyzed the coding region and short intron-exon borders of the insulin receptor substrate 1 and 2 (IRS‑1 and IRS‑2) genes in 12 cell lines derived from breast cancer (BC), 14 cell lines derived from CRC and 33 primary CRCs. The nucleotide variants identified in BC were 3 in IRS‑1, 1 of which (p.Arg267Cys) was novel and with a pathogenic potential as predicted by in silico analysis and 6 in IRS‑2. Twenty‑one variants in IRS‑1 and 18 in IRS‑2 were identified in the CRC samples. These included 11 novel IRS‑1 variants detected exclusively in CRCs, which include…

Cancer ResearchInsulin Receptor Substrate ProteinsSettore MED/06 - Oncologia MedicaIn silicoMutation MissenseBreast NeoplasmsColorectal NeoplasmBiologymedicine.disease_causeFrameshift mutationBreast cancerBreast cancerMCF-7 CellCell Line TumormedicineHumansMissense mutationFrameshift MutationInsulin Receptor Substrate ProteinSequence DeletionGeneticsMutationCaco-2 CellPolymorphism GeneticCancerGenetic VariationInsulin receptor substrate 1ArticlesGeneral MedicineInsulin receptor substrate 2HCT116 Cellsmedicine.diseaseColorectal cancerIRS1Mutagenesis InsertionalCell Transformation NeoplasticHT29 CellOncologyHCT116 CellBreast cancer; Colorectal cancer; Insulin receptor substrate 1; Insulin receptor substrate 2; Breast Neoplasms; Caco-2 Cells; Cell Line Tumor; Cell Transformation Neoplastic; Colorectal Neoplasms; Female; Frameshift Mutation; Genetic Variation; HCT116 Cells; HT29 Cells; Humans; Insulin Receptor Substrate Proteins; MCF-7 Cells; Mutagenesis Insertional; Mutation Missense; Polymorphism Genetic; Sequence Deletion; Signal Transduction; Cancer Research; OncologyInsulin Receptor Substrate ProteinsMCF-7 CellsFemaleCaco-2 CellsColorectal NeoplasmsHT29 CellsBreast NeoplasmHumanSignal Transduction
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