Search results for "Map"

showing 10 items of 3484 documents

Abstract 2484: Non-canonical Hedgehog/Gli1 signaling drives lung adenocarcinoma stem cells survival and its targeting inhibits CSC-derived tumors

2016

Abstract Introduction: Lung Adenocarcinoma (AC) is the most frequent lung cancer histological subtype and is a leading cause of cancer-related death worldwide. Hedgehog/Gli (Hh/Gli) signaling pathway regulates lung development and its aberrant activation contributes to tumor pathogenesis and play a role in cancer stem cells (CSC) control. We investigated oncogenic Hh/Gli signaling in AC-CSC. Methods: human AC-CSC were derived from primary tumors. For in vitro studies AC-CSC were maintained in serum-free medium supplemented with EGF/bFGF. For in vivo experiments, immunocompromised mice were injected with AC-CSC. Gli1 inhibitor GANT61 was used both in vitro and in vivo (IP 40 mg/kg twice/we) …

MAPK/ERK pathwayCancer Researchmedicine.medical_specialtyBiologyParacrine signallingEndocrinologyOncologyCancer stem cellGLI1Internal medicineCancer researchmedicinebiology.proteinStem cellAutocrine signallingSmoothenedHedgehogCancer Research
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Interferon-α Suppresses cAMP to Disarm Human Regulatory T Cells

2013

Abstract IFN-α is an antineoplastic agent in the treatment of several solid and hematologic malignancies that exerts strong immune- and autoimmune-stimulating activity. However, the mechanisms of immune activation by IFN-α remain incompletely understood, particularly with regard to CD4+CD25highFoxp+ regulatory T cells (Treg). Here, we show that IFN-α deactivates the suppressive function of human Treg by downregulating their intracellular cAMP level. IFN-α–mediated Treg inactivation increased CD4+ effector T-cell activation and natural killer cell tumor cytotoxicity. Mechanistically, repression of cAMP in Treg was caused by IFN-α–induced MAP–ERK kinase (MEK)/extracellular signal-regulated ki…

MAPK/ERK pathwayCancer Researchmedicine.medical_treatmentGraft vs Host DiseaseAutoimmunitychemical and pharmacologic phenomenaBiologyLymphocyte ActivationT-Lymphocytes RegulatoryNatural killer cellMiceImmune systemDownregulation and upregulationT-Lymphocyte SubsetsCyclic AMPmedicineAnimalsHumansIL-2 receptorPhosphorylationExtracellular Signal-Regulated MAP KinasesCells CulturedMitogen-Activated Protein Kinase KinasesInterleukin-2 Receptor alpha SubunitInterferon-alphaFOXP3hemic and immune systemsDNA-Binding ProteinsKiller Cells NaturalSTAT Transcription Factorsmedicine.anatomical_structureCytokineOncologyHumanized mouseImmunologyCancer researchCancer Research
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Roles of EGFR and KRAS and their downstream signaling pathways in pancreatic cancer and pancreatic cancer stem cells

2015

Pancreatic cancer is currently the fourth most common cancer, is increasing in incidence and soon will be the second leading cause of cancer death in the USA. This is a deadly malignancy with an incidence that approximates the mortality with 44,000 new cases and 36,000 deaths each year. Surgery, although only modestly successful, is the only curative option. However, due the locally aggressive nature and early metastasis, surgery can be performed on less than 20% of patients. Cytotoxic chemotherapy is palliative, has significant toxicity and improves survival very little. Thus new treatment paradigms are needed desperately. Due to the extremely high frequency of KRAS gene mutations (>90%) d…

MAPK/ERK pathwayCancer ResearchmiRsEGFRmedicine.disease_causeMetastasisProto-Oncogene Proteins p21(ras)Glycogen Synthase Kinase 3GeneticCancer stem cellKRaPancreatic cancerKRasGeneticsmedicineAnimalsHumansPTENEpidermal growth factor receptorMolecular BiologyPI3K/AKT/mTOR pathwayGSK-3biologyCancer stem cellsCancer stem cellmiRCancer stem cells; Drug resistance; EGFR; GSK-3; KRas; Metformin; miRsmedicine.diseaseMetforminErbB ReceptorsPancreatic NeoplasmsDrug resistanceNeoplastic Stem Cellsbiology.proteinCancer researchMolecular MedicineKRASSignal TransductionAdvances in Biological Regulation
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Requirement of caveolae microdomains in extracellular signal-regulated kinase and focal adhesion kinase activation induced by endothelin-1 in primary…

1999

Endothelin-1 (ET-1) mitogenic activity in astrocytes is mediated by the activation of the extracellular signal-regulated kinase (ERK) pathway together with the Rho-dependent activation of the focal adhesion kinase (FAK) pathway. To clarify the mechanisms responsible for the coordinate activation of both pathways in the ET-1 signal propagation, the involvement of caveolae microdomains, suggested to play a role in signal transduction, was evaluated. In this study, it is reported that caveolae of primary astrocytes are enriched in endothelin receptor (ETB-R). Furthermore, signaling molecules such as the adaptor proteins Shc and Grb2, and the small G protein Rho, also reside within these microd…

MAPK/ERK pathwayCaveolin 1BiologyBiochemistryCaveolinsFocal adhesionCellular and Molecular Neurosciencechemistry.chemical_compoundCaveolaeCell AdhesionAnimalsFilipinPhosphorylationCells CulturedCytoskeletonMitogen-Activated Protein Kinase 1Endothelin-1Signal transducing adaptor proteinMembrane ProteinsTyrosine phosphorylationProtein-Tyrosine KinasesActinsCell biologyAnti-Bacterial AgentsCell CompartmentationRatsEnzyme ActivationchemistryAstrocytesFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesCaveolin 1Calcium-Calmodulin-Dependent Protein Kinasesbiology.proteinTyrosineGRB2Signal transductionExtracellular SpaceCell Adhesion MoleculesSignal TransductionJournal of neurochemistry
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Emerging MEK inhibitors

2010

IMPORTANCE OF THE FIELD: The Ras/Raf/MEK/ERK pathway is often activated by genetic alterations in upstream signaling molecules. Integral components of this pathway such as Ras and B-Raf are also activated by mutation. The Ras/Raf/MEK/ERK pathway has profound effects on proliferative, apoptotic and differentiation pathways. This pathway can often be effectively silenced by MEK inhibitors. AREAS COVERED BY THIS REVIEW: This review will discuss targeting of MEK which could lead to novel methods to control abnormal proliferation which arises in cancer and other proliferative diseases. This review will cover the scientific literature from 1980 to present and is a follow on from a review which fo…

MAPK/ERK pathwayCell signalingAntineoplastic Agentsmedicine.disease_causemekerkEnzyme activatorNeoplasmsAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsHumansPharmacology (medical)Protein phosphorylationProtein Kinase InhibitorsMEK inhibitorsCell ProliferationCancerPharmacologyapoptosis; cancer; erk; kinases; mek; mek inhibitors; proliferative disorders; protein phosphorylation; signal transductionproliferative disordersMutationKinasebusiness.industryapoptosisApoptosiCancerDrugs InvestigationalMAP Kinase Kinase Kinasesmedicine.diseaseprotein phosphorylationCell biologyEnzyme ActivationTreatment OutcomekinasesChemotherapy AdjuvantRadiotherapy AdjuvantSignal transductionbusinesssignal transductionExpert Opinion on Emerging Drugs
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Regulation of ERK1/2 activity upon contact inhibition in fibroblasts.

2011

Contact inhibition is a crucial mechanism regulating proliferation in vitro and in vivo. Despite its generally accepted importance for maintaining tissue homeostasis knowledge about the underlying molecular mechanisms of contact inhibition is still scarce. Since the MAPK ERK1/2 plays a pivotal role in the control of proliferation, we investigated regulation of ERK1/2 phosphorylation which is downregulated in confluent NIH3T3 cultures. We found a decrease in upstream signaling including phosphorylation of the growth factor receptor adaptor protein ShcA and the MAPK kinase MEK1/2 in confluent compared to exponentially growing cultures whereas involvement of ERK1/2 phosphatases in ERK1/2 inact…

MAPK/ERK pathwayCell signalingBiophysicsDown-RegulationCell CommunicationBiochemistryReceptor Platelet-Derived Growth Factor betaMiceGrowth factor receptorAnimalsReceptors Platelet-Derived Growth FactorPhosphorylationMolecular BiologyTissue homeostasisCell ProliferationMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologySignal transducing adaptor proteinContact inhibitionCell BiologyFibroblastsMolecular biologyCell biologyErbB Receptorsbiology.proteinNIH 3T3 CellsPhosphorylationPlatelet-derived growth factor receptorBiochemical and biophysical research communications
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Analysis of Differentially Activated Signaling Pathways in Myeloproliferative Disease Using Kinomics Chip Profiling

2008

Abstract In a multitude of cases, oncogenic mutations are gain of function mutations that confer a constitutively activated gene product. Currently, evidence from a large body of experimental studies suggests that oncogenic transformation induced by activating kinase mutations is not sufficiently explained by constitutive kinase activation alone but is a result of aberrantly activated signaling pathways in affected cells. The JAK2V617F-mutation is a highly prevalent molecular marker in Ph-negative myeloproliferative disease (MPD). In vitro, Ba/F3-cells expressing both erythropoietin receptor (EpoR) and the JAK2V617F-mutation show constitutive activation of the JAK-STAT pathway and cytokine …

MAPK/ERK pathwayCell signalingKinaseChemistryCellular differentiationImmunologyCell BiologyHematologyTransfectionBiochemistryErythropoietin receptorCell biologyGene chip analysisSignal transductionBlood
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IAPs and cell migration.

2015

Inhibitors of apoptosis (IAPs) constitute a family of cell signaling regulators controlling several fundamental biological processes such as innate immunity, inflammation, cell death, cell proliferation, and cell differentiation. Increasing evidence from in vivo and in vitro studies indicate a function for IAPs in the modulation of invasive and migratory properties of cells. Here, we present and discuss the mechanisms whereby IAPs can control cell migration.

MAPK/ERK pathwayCell signalingProgrammed cell deathInnate immune systemCell growthCellular differentiationCell migrationCell BiologyBiologyCell biologyInhibitor of Apoptosis Proteinsbody regionsApoptosisCell MovementCancer researchCell AdhesionAnimalsHumansCytoskeletonDevelopmental BiologySignal TransductionSeminars in celldevelopmental biology
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Activity-dependent survival of developing neocortical neurons depends on PI3K signalling

2011

J. Neurochem. (2012) 120, 495–501. Abstract Spontaneous electrical network activity plays a major role in the control of cell survival in the developing brain. Several intracellular pathways are implicated in transducing electrical activity into gene expression dependent and independent survival signals. These include activation of phosphatidylinositol 3-kinase (PI3K) and its downstream effector Akt, activation of Ras and subsequently MAPK/extracellular signal-regulated kinase (MEK) and extracellular signal-regulated kinase and signalling via calcium/calmodulin-dependent protein kinase (CaMK). In the present study, we analyzed the role of these pathways for the control of neuronal survival …

MAPK/ERK pathwayCellular and Molecular NeuroscienceKinaseExtracellularBiologyProtein kinase ABiochemistryProtein kinase BCAMKPI3K/AKT/mTOR pathwayIntracellularCell biologyJournal of Neurochemistry
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Signal transduction pathways of the epidermal growth factor receptor in colorectal cancer and their inhibition by small molecules.

2012

While prognostic factors can help to classify the standard risk of subpopulations of patients with the same tumor entity, it is still not possible to predict the response of individual patients to specific therapies. The reason for such wide variation in cancer therapy responses remains largely unknown. The field of chemotherapy is currently undergoing a paradigm shift from classical cytotoxic chemotherapy to targeted therapy in order to kill tumor cells more efficiently with fewer side effects on normal tissue. In the present review, we focus on colorectal carcinoma, which is one of the most frequent tumor types worldwide and represents a leading cause of cancer-related deaths. The signali…

MAPK/ERK pathwayColorectal cancerColonmedicine.medical_treatmentAntineoplastic AgentsBiochemistryTargeted therapySmall Molecule LibrariesGrowth factor receptorDrug DiscoverymedicinePTENAnimalsHumansGrowth factor receptor inhibitorEpidermal growth factor receptorMolecular Targeted TherapyPI3K/AKT/mTOR pathwayPharmacologybiologybusiness.industryOrganic ChemistryRectummedicine.diseaseErbB ReceptorsDrug Resistance NeoplasmCancer researchbiology.proteinMolecular MedicinebusinessColorectal NeoplasmsSignal TransductionCurrent medicinal chemistry
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