Search results for "Inositol"

showing 10 items of 236 documents

An Integrative Genomic and Proteomic Analysis of PIK3CA, PTEN, and AKT Mutations in Breast Cancer

2008

Abstract Phosphatidylinositol 3-kinase (PI3K)/AKT pathway aberrations are common in cancer. By applying mass spectroscopy–based sequencing and reverse-phase protein arrays to 547 human breast cancers and 41 cell lines, we determined the subtype specificity and signaling effects of PIK3CA, AKT, and PTEN mutations and the effects of PIK3CA mutations on responsiveness to PI3K inhibition in vitro and on outcome after adjuvant tamoxifen. PIK3CA mutations were more common in hormone receptor–positive (34.5%) and HER2-positive (22.7%) than in basal-like tumors (8.3%). AKT1 (1.4%) and PTEN (2.3%) mutations were restricted to hormone receptor–positive cancers. Unlike AKT1 mutations that were absent …

ProteomicsCancer ResearchClass I Phosphatidylinositol 3-KinasesAKT1Breast NeoplasmsBiologymedicine.disease_causeArticlePhosphatidylinositol 3-KinasesBreast cancermedicineHumansPTENneoplasmsProtein kinase BPI3K/AKT/mTOR pathwayMutationPTEN PhosphohydrolaseCancerGenomicsmedicine.diseaseOncologyMutationCancer researchbiology.proteinFemaleProto-Oncogene Proteins c-aktCell DivisionTamoxifenmedicine.drugCancer Research
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Integrative analysis of cyclin protein levels identifies cyclin b1 as a classifier and predictor of outcomes in breast cancer

2009

Abstract Purpose: We studied the expression levels of cyclins B1, D1, and E1 and the implications of cyclin overexpression for patient outcomes in distinct breast cancer subtypes defined by clinical variables and transcriptional profiling. Experimental Design: The expression levels of cyclins B1, D1, and E1 were quantified in 779 breast tumors and 53 cell lines using reverse phase protein arrays and/or transcriptional profiling. Results: Whereas cyclin E1 overexpression was a specific marker of triple-negative and basal-like tumors, cyclin B1 overexpression occurred in poor prognosis hormone receptor–positive, luminal B and basal-like breast cancers. Cyclin D1 overexpression occurred in lum…

ProteomicsCancer ResearchPathologymedicine.medical_specialtyCyclin EClass I Phosphatidylinositol 3-KinasesCyclin DDNA Mutational AnalysisCyclin BBreast NeoplasmsBiologyCyclin BArticlePhosphatidylinositol 3-KinasesCyclin D1Predictive Value of TestsCell Line TumorCyclin Emedicine1-Phosphatidylinositol 3-KinaseHumansCyclin D1BreastCyclin B1Cyclin B1Oligonucleotide Array Sequence AnalysisProportional Hazards ModelsOncogene ProteinsGene Expression ProfilingCancermedicine.diseasePrognosisImmunohistochemistrySurvival AnalysisGene Expression Regulation NeoplasticCyclin E1OncologyReceptors EstrogenSpectrometry Mass Matrix-Assisted Laser Desorption-IonizationMutationCancer researchbiology.proteinFemaleBreast diseaseReceptors Progesterone
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Rho prevents apoptosis through Bcl-2 expression: Implications for interleukin-2 receptor signal transduction

1997

Here we describe a Rho-mediated apoptosis suppression pathway driven by Bcl-2 expression in the interleukin (IL)-4- or IL-2-dependent murine T cell line TS1 alpha beta. IL-2, but not IL-4, induces Bcl-2 expression through RhoA activation which is inhibited by the specific Rho family inhibitor, Clostridium difficile Toxin B, as well as by a dominant negative RhoA mutant. Using transient transfections of RhoA mutants tagged with the vesicular stomatitis virus glycoprotein, we show that a constitutively active RhoA mutant induces Bcl-2 expression and prevents apoptosis upon IL-4 withdrawal. Finally, we have identified the signaling pathway involved together with RhoA in Bcl-2 induction and sho…

RHOAImmunologyDown-RegulationClostridium difficile toxin AApoptosisClostridium difficile toxin BTransfectionCell LineMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundGTP-Binding ProteinsAnimalsHumansImmunology and AllergyPhosphatidylinositolProtein kinase AProtein Kinase CbiologyKinaseInterleukinReceptors Interleukin-2Molecular biologyCell biologyProto-Oncogene Proteins c-bcl-2chemistrybiology.proteinInterleukin-2Signal transductionrhoA GTP-Binding ProteinSignal TransductionEuropean Journal of Immunology
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α1-Adrenoceptors in the rat cerebral cortex: New insights into the characterization of α1L- and α1D-adrenoceptors

2010

36 p., figuras y tablas, bibliografía

Rat cerebral cortexAdrenergic receptorG proteinInositol PhosphatesBiologyAlpha1-adrenoceptor subtypesBinding CompetitiveCytosolReceptors Adrenergic alpha-1medicineAnimalsRNA MessengerRats WistarBinding siteInositol phosphate[3H]prazosin binding studiesCellular localizationCerebral CortexPharmacologychemistry.chemical_classificationReverse Transcriptase Polymerase Chain ReactionCell MembraneRatsCell biologyCytosolmedicine.anatomical_structureGene Expression RegulationBiochemistrychemistryAlpha1L-adrenoceptorsCerebral cortexG-proteinsFemaleGuanosine TriphosphateIntracellularAlpha1D-intracellular localizationEuropean Journal of Pharmacology
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Characterization of a Naturally Occurring Breast Cancer Subset Enriched in Epithelial-to-Mesenchymal Transition and Stem Cell Characteristics

2009

Abstract Metaplastic breast cancers (MBC) are aggressive, chemoresistant tumors characterized by lineage plasticity. To advance understanding of their pathogenesis and relatedness to other breast cancer subtypes, 28 MBCs were compared with common breast cancers using comparative genomic hybridization, transcriptional profiling, and reverse-phase protein arrays and by sequencing for common breast cancer mutations. MBCs showed unique DNA copy number aberrations compared with common breast cancers. PIK3CA mutations were detected in 9 of 19 MBCs (47.4%) versus 80 of 232 hormone receptor–positive cancers (34.5%; P = 0.32), 17 of 75 HER-2–positive samples (22.7%; P = 0.04), 20 of 240 basal-like c…

Receptors SteroidCancer ResearchPathologymedicine.medical_specialtyTranscription GeneticClass I Phosphatidylinositol 3-KinasesBreast NeoplasmsArticleCohort StudiesProto-Oncogene Proteins p21(ras)Phosphatidylinositol 3-KinasesBreast cancerProto-Oncogene ProteinsBiomarkers TumormedicineHumansRNA NeoplasmEpithelial–mesenchymal transitionskin and connective tissue diseasesComparative Genomic HybridizationMetaplasiabiologyGene Expression ProfilingCD44PTEN PhosphohydrolaseCancerEpithelial CellsMesenchymal Stem CellsSarcomaDNA NeoplasmMetaplastic Breast Carcinomamedicine.diseaseClaudin-LowOncologyMutationCarcinoma Squamous Cellras Proteinsbiology.proteinCancer researchFemaleBreast diseaseStem cellProto-Oncogene Proteins c-aktCancer Research
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Mboat7 down-regulation by hyper-insulinemia induces fat accumulation in hepatocytes.

2020

Background: Naturally occurring variation in Membrane-bound O-acyltransferase domain-containing 7 (MBOAT7), encoding for an enzyme involved in phosphatidylinositol acyl-chain remodelling, has been associated with fatty liver and hepatic disorders. Here, we examined the relationship between hepatic Mboat7 down-regulation and fat accumulation. Methods: Hepatic MBOAT7 expression was surveyed in 119 obese individuals and in experimental models. MBOAT7 was acutely silenced by antisense oligonucleotides in C57Bl/6 mice, and by CRISPR/Cas9 in HepG2 hepatocytes. Findings: In obese individuals, hepatic MBOAT7 mRNA decreased from normal liver to steatohepatitis, independently of diabetes, inflammatio…

Research paperTGFβ Transforming Growth Factor BetaIntracellular SpaceCRISPR Clustered Regularly Interspaced Short Palindromic RepeatshHEPS Human HepatocytesMice0302 clinical medicineLPIAT1DAG Diacylglyceroli.p. Intraperitonealmedia_commonFatty AcidsGeneral Medicine3. Good health030220 oncology & carcinogenesisHOMA-IR homeostasis Model Assessment of Insulin ResistanceMPO morpholinolcsh:Medicine (General)medicine.medical_specialtyPE Phosphatidyl-EthanolamineNashGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesTNFα tumor Necrosis Factor AlphaLDL Low Density LipoproteinsHyperinsulinismNAFLDSD Standard Dietmedia_common.cataloged_instanceHumansCPT1 Carnitine Palmitoyltransferase IPhosphatidylinositolGene SilencingEuropean unionVLDL Very Low Density Lipoproteinlcsh:RhHSC Human Hepatic Stellate Cellsmedicine.diseaseLipid MetabolismOA Oleic AcidCI Confidence IntervalMboat7 Membrane bound O-acyltransferase domain containing 7MCD methionine choline deficient diet030104 developmental biologyEndocrinologychemistryCDP Cytidine-DiphosphateFOXO1 Forkhead Box protein O1NAFLD nonalcoholic fatty liver diseaseSteatohepatitisBMI Body Mass IndexCL CardiolipinAcyltransferases0301 basic medicineAlcoholic liver diseaseCXCL10 C-X-C Motif Chemokine 10lcsh:Medicinechemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseIFG Impaired Fasting GlucoseAPOB Apolipoprotein BNonalcoholic fatty liver diseasePIP Phosphatidyl-Inositol-PhosphateSteatohepatitisqRT-PCR quantitative Real Time Polymerase Chain ReactionMice Knockoutlcsh:R5-920ORO Oil Red O StainingPI PhosphatidylinositolFatty liverTM6SF2 Transmembrane 6 Superfamily Member 2PhospholipidTAG TriglyceridesNASH Nonalcoholic SteatohepatitisLipogenesisLPA Lyso-Phosphatidic AcidPhosphatidylinositolSignal TransductionPS Phosphatidyl-SerinePA Palmitic AcidALD alcoholic liver diseasePC Phosphatidylcholinei.v. IntravenousFATP1 Fatty Acid Transport Protein 1Models BiologicalInternal medicinemedicineAnimalsNonalcoholic fatty liver diseasePPARα Peroxisome Proliferator-Activated Receptor alphaObesityG3P Glyceraldehyde-3-PhosphateSREBP1c Sterol Regulatory Element-Binding Protein 1HDL High Density Lipoproteinsbusiness.industryPI3K Phosphatidylinositol 3 KinaseMembrane ProteinsNHEJ Non-Homologues End JoiningPNPLA3 Patatin-like Phospholipase Domain-containing-3MTTP Microsomal Triglyceride Transfer ProteinLPIAT1 Lysophosphatidylinositol Acyltransferase 1TMC4 Transmembrane Channel-Like 4Disease Models AnimalGene Expression RegulationHepatocytesFOXA2 Forkhead Box A2mTOR mammalian target of RapamycinSteatosisInsulin ResistancebusinessPG Phosphatidyl-GlycerolFABP1 Fatty Acid-Binding Protein 1 FAS Fatty Acid SynthaseT2DM Type 2 Diabetes MellitusEBioMedicine
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Suppressor of cytokine signaling 3 sensitizes anaplastic thyroid cancer to standard chemotherapy

2009

We previously showed that cancer cells from papillary, follicular, and anaplastic thyroid carcinomas produce interleukin-4 and interleukin-10, which counteract the cytotoxic activity of conventional chemotherapy through the up-regulation of antiapoptotic molecules. Here, we identify Janus kinase/signal transducers and activators of transcription (STAT) and phosphatidyl inositol 3-kinase (PI3K)/AKT as the down-stream pathways through which these cytokines confer resistance to cell death in thyroid cancer. We found that the absence of suppressors of cytokine signaling (SOCS) molecules allows the propagation of the survival signaling. Exogenous expression of SOCS1, SOCS3, and SOCS5 in the high…

STAT3 Transcription FactorCancer ResearchCancer Research; OncologyDown-RegulationMice NudeSuppressor of Cytokine Signaling Proteinsthyroidcancer spheres cytokines apoptosis chemoterapyMicePhosphatidylinositol 3-KinasesSuppressor of Cytokine Signaling 1 ProteinMedicineAnimalsHumansSOCS3Thyroid NeoplasmsAnaplastic thyroid cancerPhosphorylationThyroid cancerPI3K/AKT/mTOR pathwayAgedSettore MED/04 - Patologia GeneraleJanus kinase 1business.industrySuppressor of cytokine signaling 1Settore BIO/16 - Anatomia UmanaGene Transfer TechniquesCancerJanus Kinase 1Middle Agedmedicine.diseaseXenograft Model Antitumor AssaysSettore MED/18 - Chirurgia GeneraleOncologyDrug Resistance NeoplasmSuppressor of Cytokine Signaling 3 ProteinImmunologyCancer researchFemalebusinessJanus kinaseSTAT6 Transcription FactorProto-Oncogene Proteins c-akt
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Effect of LIF-withdrawal on acetylcholine synthesis in the embryonic stem cell line CGR8 is not mediated by STAT3, PI3Ks or cAMP/PKA pathways.

2015

Acetylcholine (ACh) acts as a local cellular signaling molecule and is widely expressed in nature, including mammalian cells and embryonic stem cells. The murine embryonic stem cell line CGR8 synthesizes and releases substantial amounts of ACh. Particularly during early differentiation - a period associated with multiple alterations in geno-/phenotype functions - synthesis and release of ACh are increased by 10-fold. In murine stem cells second messengers of the STAT-3, PI3K and cAMP/PKA pathways are involved in maintaining self-renewal and pluripotency. The present experiments were designed to test whether blockers of these signaling pathways enhance ACh cell content in the presence of LIF…

STAT3 Transcription FactorCell signalingCurcuminMorpholinesImmunologyBiologyLeukemia Inhibitory FactorGene Expression Regulation Enzymologicchemistry.chemical_compoundMicePhosphatidylinositol 3-KinasesCyclic AMPImmunology and AllergyAnimalsLY294002PI3K/AKT/mTOR pathwayEmbryonic Stem CellsPharmacologySulfonamidesForskolinColforsinIsoquinolinesEmbryonic stem cellCyclic AMP-Dependent Protein KinasesAcetylcholineCell biologychemistryChromonesSecond messenger systemSignal transductionStem cellSignal TransductionInternational immunopharmacology
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Synergy and Antagonism of Active Constituents of ADAPT-232 on Transcriptional Level of Metabolic Regulation of Isolated Neuroglial Cells

2013

Gene expression profiling was performed on the human neuroglial cell line T98G after treatment with adaptogen ADAPT-232 and its constituents - extracts of Eleutherococcus senticosus root, Schisandra chinensis berry, and Rhodiola rosea root as well as several constituents individually, namely, eleutheroside E, schizandrin B, salidroside, triandrin, and tyrosol. A common feature for all tested adaptogens was their effect on G-protein-coupled receptor signaling pathways, i.e., cAMP, phospholipase C (PLC), and phosphatidylinositol signal transduction pathways. Adaptogens may reduce the cAMP level in brain cells by down-regulation of adenylate cyclase gene ADC2Y and up-regulation of phosphodiest…

Schisandra chinensismedicine.medical_treatmentBiologyEleutherococcus senticosusADAPT-232lcsh:RC321-571chemistry.chemical_compoundDownregulation and upregulationNeuroserpinAdaptogenmedicinePhosphatidylinositollcsh:Neurosciences. Biological psychiatry. NeuropsychiatryEleuterococcus senticosusOriginal ResearchG protein-coupled receptorpharmacogenomicsPhospholipase CGeneral Neuroscienceschizandrin BsalidrosideGene expression profilingRhodiola roseaeleutheroside EchemistryBiochemistrySignal transductionNeuroscienceFrontiers in Neuroscience
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Inhibition of FcεRI-mediated Activation of Rat Basophilic Leukemia Cells by Clostridium difficile Toxin B (Monoglucosyltransferase)

1996

Abstract Treatment of rat basophilic leukemia (RBL) 2H3-hm1 cells with Clostridium difficile toxin B (2 ng/ml), which reportedly depolymerizes the actin cytoskeleton, blocked [3H]serotonin release induced by 2,4-dinitrophenyl-bovine serum albumin, carbachol, mastoparan, and reduced ionophore A23187-stimulated degranulation by about 55-60%. In lysates of RBL cells, toxin B 14C-glucosylated two major and one minor protein. By using two-dimensional gel electrophoresis and immunoblotting, RhoA and Cdc42 were identified as protein substrates of toxin B. In contrast to toxin B, Clostridium botulinum transferase C3 that selectively inactivates RhoA by ADP-ribosylation did not inhibit degranulation…

SerotoninRHOABacterial ToxinsClostridium difficile toxin AWasp VenomsClostridium difficile toxin BBiologyCytoplasmic GranulesTritiummedicine.disease_causeBiochemistryCell LinePhosphatidylinositol 3-KinasesBacterial ProteinsTumor Cells CulturedmedicineAnimalsEnzyme InhibitorsMolecular BiologyCalcimycinAdenosine Diphosphate RiboseClostridioides difficileReceptors IgEToxinDegranulationSerum Albumin BovineCell BiologyActin cytoskeletonMolecular biologyRatsAndrostadienesKineticsPhosphotransferases (Alcohol Group Acceptor)Leukemia Basophilic AcuteBiochemistryGlucosyltransferasesMastoparanbiology.proteinIntercellular Signaling Peptides and ProteinsClostridium botulinumCarbacholCattle24-DinitrophenolPeptidesWortmanninDinitrophenolsJournal of Biological Chemistry
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