Search results for "pi3k"

showing 10 items of 240 documents

Control of ovarian steroidogenesis by insulin-like peptides in the blowfly (Phormia regina).

2004

0022–0795/04/0181–147; This study investigated the ability of insulin and of insect insulin-like peptides (ILPs) to stimulate ovarian steroidogenesis in the blowfly Phormia regina. Bovine insulin was active on ovaries isolated in vitro, which showed an age-dependent sensitivity; this peptide progressively stimulated steroidogenesis in ovaries isolated from the third day after adult molt, but not in younger ones, and had maximal activity after the fifth day. This stimulatory effect was observed equally from females reared in the presence or in the absence of males, excluding a regulatory effect of mating. The mode of action of insulin in blowflies did not involve cAMP, but triggered a specif…

medicine.medical_specialtyTime FactorsEndocrinology Diabetes and Metabolismmedicine.medical_treatmentMorpholinesEndogenyblowflychemistry.chemical_compoundPhosphatidylinositol 3-KinasesEndocrinologyOrgan Culture TechniquesInternal medicineControlmedicineAnimalsInsulinPhosphatidylinositolPI3K/AKT/mTOR pathwayPhosphoinositide-3 Kinase InhibitorsbiologyInsulinDipteraNeuropeptidesOvaryEstrogensPhormia reginabiology.organism_classificationinsulin-like peptidesIn vitroStimulation ChemicalInsulin receptorEndocrinologychemistryChromonesPhormia reginaInsect Hormonesbiology.proteinCattleFemaleovarian steroidogenesisSignal transductionThe Journal of endocrinology
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Insulin resistance aggravates atherosclerosis by reducing vascular smooth muscle cell survival and increasing CX3CL1/CX3CR1 axis.

2014

Aims Insulin resistance (IR) is a major risk factor for cardiovascular disease and atherosclerosis. Life-threatening acute events are mainly due to rupture of unstable plaques, and the role of vascular smooth muscle cells (VSMCs) in this process in IR, Type 2 diabetes mellitus, and metabolic syndrome (T2DM/MetS) has not been fully addressed. Therefore, the role of VSMC survival in the generation of unstable plaques in T2DM/MetS and the involvement of inflammatory mediators was investigated. Methods and results Defective insulin receptor substrate 2 (IRS2)-mediated signalling produced insulin-resistant VSMCs with reduced survival, migration, and higher apoptosis than control cells. Silencing…

medicine.medical_specialtyVascular smooth musclePhysiologyCell Survivalmedicine.medical_treatmentMyocytes Smooth MuscleCX3C Chemokine Receptor 1InflammationMice TransgenicBiologyMuscle Smooth VascularInsulin resistanceApolipoproteins EPhysiology (medical)Internal medicinemedicineAnimalsHumansProtein kinase BPI3K/AKT/mTOR pathwayCells CulturedMice KnockoutChemokine CX3CL1Insulinmedicine.diseaseAtherosclerosisIRS2Mice Inbred C57BLAtheromaEndocrinologyDiabetes Mellitus Type 2cardiovascular systemReceptors Chemokinemedicine.symptomInsulin ResistanceCardiology and Cardiovascular MedicineSignal TransductionCardiovascular research
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Lipid Activates mTORC1 and mTORC2 in the Absorption of Dietary Triglycerides

2018

Mechanistic target of rapamycin (mTOR) senses amino acids; however, its role in lipid metabolism is less established. Organismal lipid requirements are largely met through dietary intake. How nutrient sensing mechanisms in gut interface with dietary fat remains unclear. Here we reveal fundamental and cooperative roles for mTOR complexes 1 and 2 (mTORC1/2) in absorption of dietary triglycerides. Dietary lipid activates mTORC1/2 signaling in gut. Hyperactivating mTORC1 by deleting Tsc1 is sufficient to promote triglyceride absorption and metabolic disease in high fat-fed mice. Conversely, blocking mTORC1/2 by deleting Raptor or Rictor each decreases triglyceride absorption. Loss of Raptor seq…

medicine.medical_specialtybiologyTriglycerideChemistrydigestive oral and skin physiologyHypertriglyceridemiaDietary lipidLipid metabolismmTORC1medicine.diseasemTORC2chemistry.chemical_compoundEndocrinologyInternal medicinemedicinebiology.proteinMechanistic target of rapamycinPI3K/AKT/mTOR pathwaySSRN Electronic Journal
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FRI0150 Mtor blockade by rapamycin decreases arthritis and spondylitis development and severity in hla-b27 transgenic rats

2018

Career situation of first and presenting author Student for a master or a PhD. Introduction TNF and IL-17A have been demonstrated as key inflammatory cytokines in Spondyloarthritis (SpA), whereas targeting bone remodeling remains an unmet clinical need in SpA. The mammalian target of rapamycin (mTOR) regulates IL-17 expression and osteogenesis and could therefore be a promising therapeutic target in SpA. Objectives To investigate if blockade of mTOR with rapamycin inhibits the pathological processes in inflammation and bone in SpA. Methods Cytokines were measured by ELISA in the supernatant from SpA patient PBMCs stimulated with anti-CD3/CD28, with various concentrations of rapamycin. SpA F…

musculoskeletal diseases030203 arthritis & rheumatologyHLA-B27business.industryArthritis030209 endocrinology & metabolismInflammationPharmacologymedicine.diseaseBlockadeProinflammatory cytokineBone remodeling03 medical and health sciences0302 clinical medicinemedicineTumor necrosis factor alphamedicine.symptombusinessPI3K/AKT/mTOR pathwayFRIDAY, 15 JUNE 2018
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Targeting GSK3 and Associated Signaling Pathways Involved in Cancer

2020

Glycogen synthase kinase 3 (GSK-3) is a serine/threonine (S/T) protein kinase. Although GSK-3 originally was identified to have functions in regulation of glycogen synthase, it was subsequently determined to have roles in multiple normal biochemical processes as well as various disease conditions. GSK-3 is sometimes referred to as a moonlighting protein due to the multiple substrates and processes which it controls. Frequently, when GSK-3 phosphorylates proteins, they are targeted for degradation. GSK-3 is often considered a component of the PI3K/PTEN/AKT/GSK-3/mTORC1 pathway as GSK-3 is frequently phosphorylated by AKT which regulates its inactivation. AKT is often active in human cancer a…

natural productnatural productsmTORC1Reviewmacromolecular substancesProtein Serine-Threonine KinasesGlycogen Synthase Kinase 3GSK-3NeoplasmsHumansPhosphorylationProtein kinase AGlycogen synthaselcsh:QH301-705.5Protein kinase BWnt Signaling PathwayPI3K/AKT/mTOR pathwayGSK-3drug resistancenaturalproductsbiologyChemistryWnt signaling pathwayGeneral Medicinetargeted therapyCell biologylcsh:Biology (General)biology.proteinSignal transductionProto-Oncogene Proteins c-akt
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Capacidad predictiva y pronóstica de factores moleculares en cáncer de mama HER2 positivo tratado con quimioterapia neoadyuvante basada en antracicli…

2017

El tratamiento neoadyuvante del cáncer de mama (CM) permite estudiar marcadores subrogados que puedan predecir respuesta clínica y supervivencia. La respuesta completa patológica (RCp) definida como la ausencia de tumor infiltrante en la mama y axila en la pieza quirúrgica se asocia a mejor supervivencia. En los tumores HER2 positivo el tratamiento de elección es la combinación de quimioterapia, antraciclinas y taxanos son los esquemas con mayor evidencia, con terapia anti-HER2 (trastuzumab (TTZ)) alcanzando tasas de RCp del 30-60%. No disponemos de factores predictivos que identifiquen qué subgrupo obtendrá mayores tasas de RCp . Existe evidencia que los tumores con receptores hormonales (…

neoadyuvanciatrastuzumabPTENHER2UNESCO::CIENCIAS MÉDICAS ::Medicina del trabajo::Otrascancer de mama:CIENCIAS MÉDICAS ::Medicina del trabajo::Otras [UNESCO]PI3Kinfiltrado linfocitario
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Caracterización funcional de mutaciones oncogénicas de PI3K

2015

El cáncer es una enfermedad compleja originada por alteraciones genéticas en proto-oncogenes y/o supresores tumorales. El proto-oncogén PI3K se encuentra alterado en numerosos cánceres. La PI3K de clase I son quinasas, formadas por una subunidad catalítica (p110) y una reguladora (p85), que catalizan la conversión de PtdIns(4,5)P2 en PtdIns(3,4,5)P3 en las membranas celulares. Este último es un segundo mensajero que recluta a la quinasa de Ser/Thr AKT, la cual activa a numerosos efectores y desencadena una respuesta proliferativa y de supervivencia celular, por lo que mutaciones que causen la hiperactivación de esta ruta conllevan la transformación de células normales en células tumorales. …

p85tumorp65cáncerUNESCO::CIENCIAS DE LA VIDAPI3K:CIENCIAS DE LA VIDA [UNESCO]
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Synthesis and Antitumor Evaluation of Menthone-Derived Pyrimidine-Urea Compounds as Potential PI3K/Akt/mTOR Signaling Pathway Inhibitor.

2022

A series of novel menthone derivatives bearing pyrimidine and urea moieties was designed and synthesized to explore more potent natural product-derived antitumor agents. The structures of the target compounds were confirmed by FTIR, NMR, and HRMS. The in vitro antitumor activity was tested by standard methyl thiazolytetrazolium assay and showed that 4i, 4g, 4s, and 4m are the best compounds with IC50 values of 6.04 ± 0.62µM, 3.21 ± 0.67µM, 19.09 ± 0.49µM, and 18.68 ± 1.53µM, against Hela, MGC-803, MCF-7, and A549, respectively. The results of the preliminary action mechanism studies showed that compound 4i, the representative compound, could induce cell apoptosis in Hela cells in a dose-dep…

pyrimidineChemistrysynthesisnervous systemgenetic structuresPI3K/AKT/mTORantitumor activitymenthoneureaGeneral ChemistryQD1-999behavioral disciplines and activitiespsychological phenomena and processesFrontiers in chemistry
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A novel microtubule de-stabilizing complementarity-determining region C36L1 peptide displays antitumor activity against melanoma in vitro and in vivo

2015

AbstractShort peptide sequences from complementarity-determining regions (CDRs) of different immunoglobulins may exert anti-infective, immunomodulatory and antitumor activities regardless of the specificity of the original monoclonal antibody (mAb). In this sense, they resemble early molecules of innate immunity. C36L1 was identified as a bioactive light-chain CDR1 peptide by screening 19 conserved CDR sequences targeting murine B16F10-Nex2 melanoma. The 17-amino acid peptide is readily taken up by melanoma cells and acts on microtubules causing depolymerization, stress of the endoplasmic reticulum and intrinsic apoptosis. At low concentrations, C36L1 inhibited migration, invasion and proli…

rho GTP-Binding ProteinsMelanoma ExperimentalAntineoplastic AgentsApoptosisPeptideComplementarity determining regionBiologyEndoplasmic ReticulumMicrotubulesArticleMicePhosphatidylinositol 3-KinasesCell MovementTubulinCell Line TumormedicineAnimalsNeoplasm MetastasisMelanomaPI3K/AKT/mTOR pathwayCell Proliferationchemistry.chemical_classificationMultidisciplinaryInnate immune systemCell growthMelanomaIntrinsic apoptosisPTEN Phosphohydrolasemedicine.diseaseComplementarity Determining RegionsMolecular biologyMitochondriaDisease Models AnimalchemistryCell cultureCancer researchProtein MultimerizationPeptidesProto-Oncogene Proteins c-aktSignal TransductionScientific Reports
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MTOR inhibitor-based combination therapies for pancreatic cancer

2018

Background: Although the mechanistic target of rapamycin (MTOR) kinase, included in the mTORC1 and mTORC2 signalling hubs, has been demonstrated to be active in a significant fraction of patients with pancreatic ductal adenocarcinoma (PDAC), the value of the kinase as a therapeutic target needs further clarification. Methods: We used Mtor floxed mice to analyse the function of the kinase in context of the pancreas at the genetic level. Using a dual-recombinase system, which is based on the flippase-FRT (Flp-FRT) and Cre-loxP recombination technologies, we generated a novel cellular model, allowing the genetic analysis of MTOR functions in tumour maintenance. Cross-species validation and pha…

therapeutic resistance0301 basic medicineCancer ResearchCell SurvivalMAP Kinase Signaling Systempancreatic cancerAntineoplastic AgentsContext (language use)Mechanistic Target of Rapamycin Complex 2mTORC1Mechanistic Target of Rapamycin Complex 1BiologymTORC2BortezomibMice03 medical and health sciencesCell Line TumorPancreatic cancermedicineAnimalsHumansExtracellular Signal-Regulated MAP KinasesMechanistic target of rapamycinPI3K/AKT/mTOR pathwayBenzoxazolesKinaseMTORTOR Serine-Threonine Kinasesmedicine.diseaseddc:3. Good healthPancreatic NeoplasmsPyrimidines030104 developmental biologyOncologybiology.proteinCancer researchCamptothecinTOR Serine-Threonine KinasesPhosphatidylinositol 3-KinaseTranslational TherapeuticsProto-Oncogene Proteins c-aktBiologieCarcinoma Pancreatic Ductal
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