Search results for "Inositol"

showing 10 items of 236 documents

Influences of TP53 and the anti-aging DDR1 receptor in controlling Raf/MEK/ERK and PI3K/Akt expression and chemotherapeutic drug sensitivity in prost…

2020

Background TP53 plays critical roles in sensitivity to chemotherapy, and aging. Collagen is very important in aging. The molecular structure and biochemical properties of collagen changes during aging. The discoidin domain receptor (DDR1) is regulated in part by collagen. Elucidating the links between TP53 and DDR1 in chemosensitivity and aging could improve therapies against cancer and aging. Results Restoration of WT-TP53 activity resulted in increased sensitivity to chemotherapeutic drugs and elevated expression of key components of the Raf/MEK/ERK, PI3K/Akt and DDR1 pathways. DDR1 could modulate the levels of Raf/MEK/ERK and PI3K/Akt pathways as well as sensitize the cells to chemothera…

MAPK/ERK pathwayMalecollagenAgingRAF/MEK/ERKMAP Kinase Signaling SystemAntineoplastic Agentsdiscoidin domain receptor (DDR1)DDRCollagen receptorPhosphatidylinositol 3-KinasesDiscoidin Domain Receptor 1Cell Line TumorHumansRapamycinTP53ReceptorProtein kinase BPI3K/AKT/mTOR pathwayDDR1ChemistryWild typeProstateProstatic NeoplasmschemoresistanceCell Biologyprostate cancerDrug Resistance NeoplasmMutationCancer researchraf KinasesTumor Suppressor Protein p53Discoidin domainResearch Paper
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Therapeutic resistance resulting from mutations in Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR signaling pathways.

2011

Chemotherapy remains a commonly used therapeutic approach for many cancers. Indeed chemotherapy is relatively effective for treatment of certain cancers and it may be the only therapy (besides radiotherapy) that is appropriate for certain cancers. However, a common problem with chemotherapy is the development of drug resistance. Many studies on the mechanisms of drug resistance concentrated on the expression of membrane transporters and how they could be aberrantly regulated in drug resistant cells. Attempts were made to isolate specific inhibitors which could be used to treat drug resistant patients. Unfortunately most of these drug transporter inhibitors have not proven effective for ther…

MAPK/ERK pathwayPTENTumor suppressor genekinase inhibitorPhysiologymedicine.medical_treatmentClinical Biochemistrygrowth factor receptorAntineoplastic AgentsDrug resistancePharmacologyBiologyTargeted therapy03 medical and health sciencesMicePhosphatidylinositol 3-Kinases0302 clinical medicineGrowth factor receptormedicinePTENAnimalsHumansExtracellular Signal-Regulated MAP KinasesProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesTOR Serine-Threonine KinasesPTEN PhosphohydrolaseCell BiologyMAP Kinase Kinase Kinases3. Good healthErbB ReceptorsDrug Resistance Neoplasm030220 oncology & carcinogenesisMutationCancer researchbiology.proteinraf KinasesProto-Oncogene Proteins c-aktDrug resistance therapeutic sensitivity targeted therapy RAF ERKACUTE MYELOID LEUKAEMIASignal TransductionJournal of cellular physiology
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Mutations and Deregulation of Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR Cascades Which Alter Therapy Response.

2012

The Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascades are often activated by genetic alterations in upstream signaling molecules such as receptor tyrosine kinases (RTK). Certain components of these pathways, RAS, NF1, BRAF, MEK1, DUSP5, PP2A, PIK3CA, PIK3R1, PIK3R4, PIK3R5, IRS4, AKT, NFKB1, MTOR, PTEN, TSC1, and TSC2 may also be activated/inactivated by mutations or epigenetic silencing. Upstream mutations in one signaling pathway or even in downstream components of the same pathway can alter the sensitivity of the cells to certain small molecule inhibitors. These pathways have profound effects on proliferative, apoptotic and differentiation pathways. Dysregulation of components of these cas…

MAPK/ERK pathwayPremature agingMAP Kinase Signaling SystemTargeted Therapy Therapy Resistance Mutations Raf Akt PI3K mTORMtorReviewsPi3kPI3KReceptor tyrosine kinaseAkt; Mtor; Mutations; Pi3k; Raf; Targeted therapy; Therapy resistance;Targeted therapyPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineAnimalsHumansPTENExtracellular Signal-Regulated MAP KinasesProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesbiologyChemistryTOR Serine-Threonine KinasesAktTherapy resistancePTEN PhosphohydrolaseTargeted TherapyTherapy ResistanceRafProtein phosphatase 2MAP Kinase Kinase Kinases3. Good healthCell biologyOncology030220 oncology & carcinogenesisMutationras ProteinsmTORCancer researchbiology.proteinraf KinasesMitogen-Activated Protein KinasesSignal transductionProto-Oncogene Proteins c-aktMutationsSignal TransductionOncotarget
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a1D-Adrenoceptors are responsible for the high sensitivity and the slow time-course of noradrenaline-mediated contraction in conductance arteries.

2013

The objective of this study was to determine whether the different time-course characteristics of α1-adrenoceptor-mediated contraction in arteries can be related to the subtypes involved. Contractile responses to noradrenaline (NA) were compared with inositol phosphate accumulation and extracellular signal-regulated kinase (ERK)1/2 phosphorylation after α1-agonist stimuli in the same vessels in the presence or absence of α1-antagonists in rat or in α1-subtype knockout (KO) mice. Aorta, where α1D-AR is the main functional subtype, had higher sensitivity to NA (in respect of inositol phosphate [IP], pERK1/2, and contractile response) than tail artery, where the α1A-adrenoceptor subtype is pre…

MAPK/ERK pathwaychemistry.chemical_classificationAgonistmedicine.medical_specialtyAortaContraction (grammar)business.industryKinasemedicine.drug_classcontraction time-courseconductance and resistance vesselsOriginal ArticlesEndocrinologyNeurologychemistryInternal medicinemedicine.arterymedicineExtracellularPhosphorylationGeneral Pharmacology Toxicology and Pharmaceuticsconductance and resistance vessels contraction time-course a1A-adrenoceptorsα1A-adrenoceptorsInositol phosphatebusiness
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Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR cascade inhibitors: How mutations can result in therapy resistance and how to overcome resistance

2012

// James A. McCubrey 1 , Linda S. Steelman 1 , William H. Chappell 1 , Stephen L. Abrams 1 , Richard A. Franklin 1 , Giuseppe Montalto 2 , Melchiorre Cervello 3 , Massimo Libra 4 , Saverio Candido 4 , Grazia Malaponte 4 , Maria C. Mazzarino 4 , Paolo Fagone 4 , Ferdinando Nicoletti 4 , Jorg Basecke 5 , Sanja Mijatovic 6 , Danijela Maksimovic-Ivanic 6 , Michele Milella 7 , Agostino Tafuri 8 , Francesca Chiarini 9 , Camilla Evangelisti 9 , Lucio Cocco 10 , Alberto M. Martelli 9,10 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC, USA 2 Department of Internal Medicine and Specialties, University of Palermo, Palermo, Italy 3 Consi…

MAPK/ERK pathwaymedicine.medical_treatmentPI3KTargeted therapyTargeted therapyPhosphatidylinositol 3-Kinases0302 clinical medicineNeoplasmsTreatment resistanceExtracellular Signal-Regulated MAP KinasesPhosphoinositide-3 Kinase InhibitorsGenetics0303 health sciencesbiologyCancer stem cellsTOR Serine-Threonine KinasesMAP Kinase Kinase KinasesDiscovery and development of mTOR inhibitorshumanities3. Good healthOncology030220 oncology & carcinogenesismTORSignal TransductionProto-Oncogene Proteins B-rafReviewsAntineoplastic Agents03 medical and health sciencesCell Line TumormedicineHumansPTENProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biologybusiness.industryAkt; Cancer stem cells; mTOR; PI3K; Raf; Targeted therapy; Therapy resistanceAktPTEN PhosphohydrolaseTherapy resistanceRafProtein phosphatase 2Targeted Therapy Therapy Resistance Cancer Stem Cells Raf Akt PI3K mTORDrug Resistance NeoplasmMutationras ProteinsCancer researchbiology.proteinbusinessProto-Oncogene Proteins c-akt
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Enhanced proinflammatory response to the Candida albicans gpi7 null mutant by murine cells.

2008

International audience; The Candida albicans gpi7/gpi7 null mutant strain (Deltagpi7), which is affected in glycosylphosphatidylinositol (GPI) anchor biosynthesis, showed a reduced virulence following systemic infection of C57BL/6 mice. In vitro production of TNF-alpha, IL-6 and IL-1beta by macrophages in response to Deltagpi7 cells was significantly increased as compared to control (wild type GPI7/GPI7 and revertant gpi7/GPI7) cells; this probably contributes to the enhanced recruitment of neutrophils to the peritoneal cavity in response to Deltagpi7 cells. Survival of knockout mice for Toll-like receptor (TLR) 2 and TLR4 following intravenous injection of Deltagpi7 cells showed no signifi…

MESH: InflammationGlycosylphosphatidylinositolsNeutrophilsmedicine.medical_treatmentInterleukin-1betasourisMESH: NeutrophilsMESH: VirulenceMESH: Mice KnockoutMiceMESH: Interleukin-1betaNull cellMESH: AnimalsCandida albicansPeritoneal CavityCells CulturedMice Knockout0303 health sciencesToll-like receptorbiologyVirulenceMESH: Toll-Like Receptor 2MESH: Peritoneal CavityMESH: Toll-Like Receptor 4MESH: GlycosylphosphatidylinositolsInfectious DiseasesCytokineMESH: Survival AnalysisTumor necrosis factor alphaMESH: Fungal Proteinsprotéine de la paroi cellulaireMESH: Macrophages PeritonealMESH: Cells CulturedVirulence FactorsImmunologyMicrobiologyMicrobiologyProinflammatory cytokineFungal Proteins03 medical and health sciencesMESH: Mice Inbred C57BLmedicineAnimalsMESH: Mice030304 developmental biologyMESH: Virulence FactorsInflammation030306 microbiologyInterleukin-6Tumor Necrosis Factor-alphaMESH: Candida albicans[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologybiology.organism_classificationSurvival AnalysispathogénicitéMESH: Interleukin-6Toll-Like Receptor 2Mice Inbred C57BLToll-Like Receptor 4TLR2GlycosylphosphatidylinositolMESH: Gene DeletionMESH: Tumor Necrosis Factor-alphaTLR4Macrophages Peritonealcandida albicansimmunitéGene Deletion
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Colony-stimulating factor-1-induced oscillations in phosphatidylinositol-3 kinase/AKT are required for caspase activation in monocytes undergoing dif…

2009

Abstract The differentiation of human peripheral blood monocytes into resident macrophages is driven by colony-stimulating factor-1 (CSF-1), which upon interaction with CSF-1 receptor (CSF-1R) induces within minutes the phosphorylation of its cytoplasmic tyrosine residues and the activation of multiple signaling complexes. Caspase-8 and -3 are activated at day 2 to 3 and contribute to macrophage differentiation, for example, through cleavage of nucleophosmin. Here, we show that the phosphatidylinositol-3 kinase and the downstream serine/threonine kinase AKT connect CSF-1R activation to caspase-8 cleavage. Most importantly, we demonstrate that successive waves of AKT activation with increasi…

Macrophage colony-stimulating factorCellular differentiationImmunologyImmunoblottingApoptosisBiologyBiochemistryMonocytesImmunoenzyme TechniquesPhosphatidylinositol 3-KinasesHumansImmunoprecipitationRNA MessengerPhosphorylationProtein kinase BCells CulturedPhosphoinositide-3 Kinase InhibitorsMitogen-Activated Protein Kinase 1Caspase 8Mitogen-Activated Protein Kinase 3MAP kinase kinase kinaseKinaseAkt/PKB signaling pathwayReverse Transcriptase Polymerase Chain ReactionMacrophage Colony-Stimulating FactorMacrophagesCell DifferentiationCell BiologyHematologyFlow CytometryCell biologyEnzyme ActivationPhosphorylationSignal transductionProto-Oncogene Proteins c-aktSignal TransductionBlood
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Physiological relevance of the neuronal isoform of inositol-1,4,5-trisphosphate 3-kinases in mice

2020

Inositol-1,4,5-trisphosphate 3-kinase-A (ITPKA) is the neuronal isoform of ITPKs and exhibits both actin bundling and InsP3kinase activity. In addition to neurons, ITPKA is ectopically expressed in tumor cells, where its oncogenic activity increases tumor cell malignancy. In order to analyze the physiological relevance of ITPKA, here we performed a broad phenotypic screening of itpka deficient mice. Our data show that among the neurobehavioral tests analyzed, itpka deficient mice reacted faster to a hotplate, prepulse inhibition was impaired and the accelerating rotarod test showed decreased latency of itpka deficient mice to fall. These data indicate that ITPKA is involved in the regulatio…

Male0301 basic medicineGene isoformCentral nervous systemMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicinegenetics [Phosphotransferases (Alcohol Group Acceptor)]medicinephysiology [Prepulse Inhibition]AnimalsHumansdeficiency [Phosphotransferases (Alcohol Group Acceptor)]Inositolddc:610Prepulse inhibitionActinMice KnockoutNeuronsenzymology [Neurons]Prepulse InhibitionChemistryKinaseGeneral Neurosciencedeficiency [Isoenzymes]Small intestineCell biologyIsoenzymesPhosphotransferases (Alcohol Group Acceptor)030104 developmental biologymedicine.anatomical_structureCell cultureFemaleCaco-2 Cellsgenetics [Isoenzymes]030217 neurology & neurosurgeryNeuroscience Letters
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Molecular mechanisms mediating the neuroprotective role of the selective estrogen receptor modulator, bazedoxifene, in acute ischemic stroke: A compa…

2017

As the knowledge on the estrogenic system in the brain grows, the possibilities to modulate it in order to afford further neuroprotection in brain damaging disorders so do it. We have previously demonstrated the ability of the selective estrogen receptor modulator, bazedoxifene (BZA), to reduce experimental ischemic brain damage. The present study has been designed to gain insight into the molecular mechanisms involved in such a neuroprotective action by investigating: 1) stroke-induced apoptotic cell death; 2) expression of estrogen receptors (ER) ERα, ERβ and the G-protein coupled estrogen receptor (GPER); and 3) modulation of MAPK/ ERK1/2 and PI3K/Akt signaling pathways. For comparison, …

Male0301 basic medicineMAPK/ERK pathwayIndolesSignaling pathwaysEndocrinology Diabetes and MetabolismClinical BiochemistryEstrogen receptorApoptosisEstrogen receptorsSecond Messenger SystemsBiochemistryBrain IschemiaReceptors G-Protein-Coupled0302 clinical medicineEndocrinologyPhosphatidylinositol PhosphatesCerebral CortexNeuronsEstradiolNeuroprotectionStrokeNeuroprotective AgentsSelective estrogen receptor modulatorReperfusion InjuryMolecular MedicineSelective estrogen receptor modulatorsGPERmedicine.medical_specialtyMAP Kinase Signaling Systemmedicine.drug_classAcute ischemic strokeNerve Tissue ProteinsBazedoxifeneBiologyNeuroprotection03 medical and health sciencesInternal medicinemedicineAnimalsEstrogen Receptor betaRats WistarMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayEstrogen Receptor alphaEstrogensCell BiologyEstrogen030104 developmental biologyEndocrinologyEstrogen030217 neurology & neurosurgeryThe Journal of Steroid Biochemistry and Molecular Biology
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Small Bowel Carcinomas in Coeliac or Crohn’s Disease: Clinico-pathological, Molecular, and Prognostic Features. A Study From the Small Bowel Cancer I…

2017

Background and aims An increased risk of small bowel carcinoma [SBC] has been reported in coeliac disease [CD] and Crohn's disease [CrD]. We explored clinico-pathological, molecular, and prognostic features of CD-associated SBC [CD-SBC] and CrD-associated SBC [CrD-SBC] in comparison with sporadic SBC [spo-SBC]. Methods A total of 76 patients undergoing surgical resection for non-familial SBC [26 CD-SBC, 25 CrD-SBC, 25 spo-SBC] were retrospectively enrolled to investigate patients' survival and histological and molecular features including microsatellite instability [MSI] and KRAS/NRAS, BRAF, PIK3CA, TP53, HER2 gene alterations. Results CD-SBC showed a significantly better sex-, age-, and st…

Male0301 basic medicineNeuroblastoma RAS viral oncogene homologOncologySurvivalReceptor ErbB-2Colorectal cancermedicine.disease_causeInflammatory bowel diseaseInflammatory bowel diseasetumour-infiltrating lymphocyteErbB-20302 clinical medicineCrohn DiseaseRetrospective StudieRisk Factors80 and overChildClass I Phosphatidylinositol 3-KinaseAged 80 and overColonic NeoplasmSettore MED/12 - GastroenterologiaCrohn's diseaseMLH1 methylationTumour-infiltrating lymphocytesGastroenterologyGeneral MedicineMiddle AgedPrognosisInflammatory bowel disease; Microsatellite instability; MLH1 promoter methylation; Survival; Tumour-infiltrating lymphocytes; Gastroenterology030220 oncology & carcinogenesisColonic NeoplasmsSurvival AnalysiKRASHumanReceptorAdultProto-Oncogene Proteins B-rafmedicine.medical_specialtyPrognosiClass I Phosphatidylinositol 3-KinasesSettore MED/08 - Anatomia PatologicaNOProto-Oncogene Proteins p21(ras)MLH1 promoter methylationYoung Adult03 medical and health sciencesInternal medicinemedicineCarcinomaHumansMLH1 methylation; inflammatory bowel disease; microsatellite instability; survival; tumour-infiltrating lymphocytesneoplasmsAgedRetrospective StudiesInflammatory bowel disease; Microsatellite instability; MLH1 promoter methylation; Survival; Tumour-infiltrating lymphocytes; Adult; Aged; Aged 80 and over; Celiac Disease; Child; Class I Phosphatidylinositol 3-Kinases; Colonic Neoplasms; Crohn Disease; Humans; Male; Microsatellite Instability; Middle Aged; Prognosis; Proto-Oncogene Proteins B-raf; Proto-Oncogene Proteins p21(ras); Receptor ErbB-2; Retrospective Studies; Risk Factors; Survival Analysis; Tumor Suppressor Protein p53; Young Adult; Gastroenterologybusiness.industryTumour-infiltrating lymphocyteRisk FactorCancerMicrosatellite instabilityinflammatory bowel disease; microsatellite instability; MLH1 promoter methylation; tumour-infiltrating lymphocytes; survivalmedicine.diseaseSurvival Analysiseye diseasesdigestive system diseasesCeliac Disease030104 developmental biologyMicrosatellite instabilityTumor Suppressor Protein p53businessJournal of Crohn's and Colitis
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