Search results for "mTORC1"

showing 10 items of 23 documents

Mechanisms of action of metformin in type 2 diabetes: Effects on mitochondria and leukocyte-endothelium interactions.

2020

Type 2 diabetes (T2D) is a very prevalent, multisystemic, chronic metabolic disorder closely related to atherosclerosis and cardiovascular diseases. It is characterised by mitochondrial dysfunction and the presence of oxidative stress. Metformin is one of the safest and most effective anti-hyperglycaemic agents currently employed as first-line oral therapy for T2D. It has demonstrated additional beneficial effects, unrelated to its hypoglycaemic action, on weight loss and several diseases, such as cancer, cardiovascular disorders and metabolic diseases, including thyroid diseases. Despite the vast clinical experience gained over several decades of use, the mechanism of action of metformin i…

0301 basic medicineAdvanced glycation end product (AGE)AMP-activated protein kinase (AMPK)endocrine system diseasesglycerol 3-phosphate dehydrogenase (GPD)Clinical Biochemistrytype 1 diabetes (T1D)Type 2 diabetesmTORC1Review Articleelectron transport chain (ETC)PharmacologyMitochondrionmedicine.disease_causeBiochemistry0302 clinical medicineLeukocytesCREB-binding protein (CBP)inner mitochondrial membrane (IMM)lcsh:QH301-705.5lcsh:R5-920cAMP response element-binding (CREB)glucagon-like peptide 1 (GLP-1)type 2 diabetes (T2D)Type 2 diabetesMetforminMetforminMitochondriamedicine.anatomical_structurereactive nitrogen species (RNS)reactive oxygen species (ROS)sirtuin (SIRT)medicine.symptomlcsh:Medicine (General)cardiovascular diseases (CVD)medicine.drugEndotheliumnitric oxide synthase (NOS)polycystic ovary syndrome (PCOS)Pathophysiologyinsulin resistance (IR)superoxide dismutase (SOD)03 medical and health sciencesglycated haemoglobin (HbA1c)medicineorganic cation transporter (OCT)HumansEndotheliumintercellular adhesion molecule-1 (ICAM-1)business.industryoxidative phosphorylation (OXPHOS)Organic Chemistryperoxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)AMPKmedicine.diseaseAtherosclerosisvascular cell adhesion molecule-1 (VCAM-1)Treatment030104 developmental biologylcsh:Biology (General)Mechanism of actionDiabetes Mellitus Type 2Oxidative stressbusinessinsulin receptor substrate (IRS)030217 neurology & neurosurgeryOxidative stress
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Regulation of GSK-3 activity by curcumin, berberine and resveratrol: Potential effects on multiple diseases.

2017

Natural products or nutraceuticals promote anti-aging, anti-cancer and other health-enhancing effects. A key target of the effects of natural products may be the regulation of the PI3K/PTEN/Akt/mTORC1/GSK-3 pathway. This review will focus on the effects of curcumin (CUR), berberine (BBR) and resveratrol (RES), on the PI3K/PTEN/Akt/mTORC1/GSK-3 pathway, with a special focus on GSK-3. These natural products may regulate the pathway by multiple mechanisms including: reactive oxygen species (ROS), cytokine receptors, mirco-RNAs (miRs) and many others. CUR is present the root of turmeric (Curcuma longa). CUR is used in the treatment of many disorders, especially in those involving inflammatory p…

0301 basic medicineCancer ResearchCurcuminBerberinemTORC1PharmacologyResveratrolMechanistic Target of Rapamycin Complex 1Protective AgentsNatural product03 medical and health scienceschemistry.chemical_compoundGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesBerberineGeneticNeoplasmsOsteoarthritisStilbenesGeneticsPTENHumansCurcumaMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwayInflammationNatural productsbiologyBerberine; Curcumin; Natural products; ResveratrolPTEN PhosphohydrolaseNeurodegenerative Diseasesbiology.organism_classification030104 developmental biologyBiochemistrychemistryGene Expression RegulationCardiovascular DiseasesResveratrolbiology.proteinCurcuminMolecular MedicineProto-Oncogene Proteins c-aktSignal Transduction
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RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1 and TP53 pathways and regulatory miRs as therapeutic targets in hepatocellular carcinoma

2019

Introduction: Hepatocellular carcinoma (HCC) is a significant problem globally because of viral infections and the increasing incidence of obesity and fatty liver disease. However, it is difficult to treat because its inherent genetic heterogeneity results in activation of numerous signaling pathways. Kinases have been targeted for decades with varying results, but the development of therapeutic resistance is a major challenge. Areas covered: The key roles of the RAS/RAF/MEK/ERK, PI3K/PTEN/AKT/mTORC1, TP53 microRNAs (miRs) as therapeutic targets are discussed and we suggests novel approaches for targeting miRs or their downstream targets to combat HCC. We performed literature searches using…

0301 basic medicineMAPK/ERK pathwayCarcinoma HepatocellularHepatocellular carcinmamedicine.medical_treatmentClinical BiochemistryAntineoplastic AgentsmTORC1signal transduction inhibitorsTargeted therapy03 medical and health sciences0302 clinical medicineDrug DiscoverymicroRNAmedicinePTENAnimalsHumanscancerMolecular Targeted TherapyTP53HCCRAS/RAF/MEK/ERKProtein kinase BPI3K/AKT/mTOR pathwaymiRNAPharmacologybiologybusiness.industryKinaseLiver NeoplasmsMirhepatocellular carcinomatargeted therapyGene Expression Regulation NeoplasticMicroRNAssignal transduction inhibitor030104 developmental biologyDrug Resistance Neoplasm030220 oncology & carcinogenesisbiology.proteinCancer researchMolecular MedicinePI3K/PTEN/AKTbusinessSignal Transduction
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Dietary protein restriction reduces circulating VLDL triglyceride levels via CREBH-APOA5-dependent and -independent mechanisms

2018

Hypertriglyceridemia is an independent risk factor for cardiovascular disease. Dietary interventions based on protein restriction (PR) reduce circulating triglycerides (TGs), but underlying mechanisms and clinical relevance remain unclear. Here, we show that 1 week of a protein-free diet without enforced calorie restriction significantly lowered circulating TGs in both lean and diet-induced obese mice. Mechanistically, the TG-lowering effect of PR was due, in part, to changes in very low-density lipoprotein (VLDL) metabolism both in liver and peripheral tissues. In the periphery, PR stimulated VLDL-TG consumption by increasing VLDL-bound APOA5 expression and promoting VLDL-TG hydrolysis and…

0301 basic medicineMalemedicine.medical_specialtyVery low-density lipoproteinDietary proteinFGF21Calorie restrictionmTORC1Lipoproteins VLDLMechanistic Target of Rapamycin Complex 1Protein Serine-Threonine Kinases03 medical and health sciencesMice0302 clinical medicineRisk FactorsInternal medicinemedicineDiet Protein-RestrictedIntegrated stress responseAnimalsHumansCyclic AMP Response Element-Binding ProteinTriglyceridesRandomized Controlled Trials as TopicHypertriglyceridemiaChemistryHydrolysisHypertriglyceridemianutritional and metabolic diseasesGeneral Medicinemedicine.diseaseLipid Metabolism030104 developmental biologyEndocrinologyApolipoproteinsHypotriglyceridemiaLiverApolipoprotein A-Vlipids (amino acids peptides and proteins)Female030217 neurology & neurosurgeryLipoproteinResearch Article
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A Stat6/Pten Axis Links Regulatory T Cells with Adipose Tissue Function

2017

Obesity and type 2 diabetes are associated with metabolic defects and adipose tissue inflammation. Foxp3(+) regulatory T cells (Tregs) control tissue homeostasis by counteracting local inflammation. However, if and how T cells interlink environmental influences with adipocyte function remains unknown. Here, we report that enhancing sympathetic tone by cold exposure, beta3-adrenergic receptor (ADRB3) stimulation or a short-term high-calorie diet enhances Treg induction in vitro and in vivo. CD4(+) T cell proteomes revealed higher expression of Foxp3 regulatory networks in response to cold or ADRB3 stimulation in vivo reflecting Treg induction. Specifically, Ragulator-interacting protein C17o…

0301 basic medicinePTENProteomePhysiologyAdipose tissueStimulationmTORC1Diet induced thermogenesisBorcs6 ; C17orf59 ; Foxp3 ; Pten ; Stat6 ; T Cells ; Tregs ; Adipose Tissue Function ; Cold Exposure ; Metabolic Function ; Metabolism ; Regulatory T cellsT-Lymphocytes Regulatorychemistry.chemical_compound0302 clinical medicineAdipose Tissue BrownAdipocyteUncoupling Protein 1Tissue homeostasisSTAT6ddc:616Mice Inbred BALB CFOXP3Forkhead Transcription Factorshemic and immune systemsRegulatory T cellsCell biologyCold TemperatureFoxp3FemaleMetabolic functionmedicine.symptomSignal TransductionBorcs6Adipose Tissue WhiteCold exposureT cellsTregschemical and pharmacologic phenomenaInflammationBiologyArticle03 medical and health sciencesReceptors Adrenergic betaAdipose tissue functionmedicineAnimalsC17orf59Molecular BiologyPTEN PhosphohydrolaseCell BiologyMetabolism030104 developmental biologychemistryImmunologySTAT6 Transcription Factor030217 neurology & neurosurgeryCell Metabolism
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The Intracellular Cleavage Product of the NG2 Proteoglycan Modulates Translation and Cell-Cycle Kinetics via Effects on mTORC1/FMRP Signaling

2018

The NG2 proteoglycan is expressed by oligodendrocyte precursor cells (OPCs) and is abundantly expressed by tumors such as melanoma and glioblastoma. Functions of NG2 include an influence on proliferation, migration and neuromodulation. Similar to other type-1 membrane proteins, NG2 undergoes proteolysis, generating a large ectodomain, a C-terminal fragment (CTF) and an intracellular domain (ICD) via sequential action of α- and γ-secretases which is enhanced by neuronal activity. Functional roles of NG2 have so far been shown for the full-length protein, the released ectodomain and CTF, but not for the ICD. In this study, we characterized the role of the NG2 ICD in OPC and Human Embryonic Ki…

0301 basic medicinePopulationP70-S6 Kinase 1mTORC1γ-secretaselcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceNG2educationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryPI3K/AKT/mTOR pathwayOriginal Researcheducation.field_of_studyChemistryICDHEK 293 cellsTranslation (biology)S6K1Cell biologystomatognathic diseases030104 developmental biologyEctodomainnervous systemeEF2mTORPhosphorylationFMRPOPCNeuroscienceFrontiers in Cellular Neuroscience
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Metformin influences drug sensitivity in pancreatic cancer cells

2018

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive, highly metastatic malignancy and accounts for 85% of pancreatic cancers. PDAC patients have poor prognosis with a five-year survival of only 5–10% after diagnosis and treatment. Pancreatic cancer has been associated with type II diabetes as the frequency of recently diagnosed diabetics that develop pancreatic cancer within a 10-year period of initial diagnosis of diabetes in increased in comparison to non-diabetic patients. Metformin is a very frequently prescribed drug used to treat type II diabetes. Metformin acts in part by stimulating AMP-kinase (AMPK) and results in the suppression of mTORC1 activity and the induction o…

AMPK0301 basic medicineCancer Researchendocrine system diseases03 medical and health sciencesPancreatic cancerGeneticsMedicineAnimalsHumansDoxorubicinDrug InteractionsRapamycinSignal transduction inhibitormTORC1Molecular BiologyCisplatinSirolimusAnimalbusiness.industryPancreatic NeoplasmCancermedicine.diseaseGemcitabineMetforminMetforminPancreatic Neoplasms030104 developmental biologyDrug InteractionDocetaxelDiabetes Mellitus Type 2SirolimusCancer researchMolecular MedicinebusinessHumanmedicine.drugCarcinoma Pancreatic DuctalSignal Transduction
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p62: Friend or Foe? Evidences for OncoJanus and NeuroJanus Roles

2020

p62 is a versatile protein involved in the delicate balance between cell death and survival, which is fundamental for cell fate decision in the context of both cancer and neurodegenerative diseases. As an autophagy adaptor, p62 recognizes polyubiquitin chains and interacts with LC3, thereby targeting the selected cargo to the autophagosome with consequent autophagic degradation. Beside this function, p62 behaves as an interactive hub in multiple signalling including those mediated by Nrf2, NF-κB, caspase-8, and mTORC1. The protein is thus crucial for the control of oxidative stress, inflammation and cell survival, apoptosis, and metabolic reprogramming, respectively. As a multifunctional pr…

AutophagosomeProgrammed cell deathP62ApoptosisContext (language use)mTORC1Cell fate determinationBiologyCatalysislcsh:ChemistryInorganic ChemistryStress granuleAutophagymedicinePhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyCancerNeurodegenerative diseasesOrganic ChemistryNeurodegenerationAutophagyGeneral Medicinemedicine.diseaseComputer Science ApplicationsCell biologylcsh:Biology (General)lcsh:QD1-999International Journal of Molecular Sciences
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Sprint and Strength Training Modulates Autophagy and Proteostasis in Aging Sprinters

2020

Purpose Exercise and aging may modulate muscle protein homeostasis and autophagy, but few studies examine highly-trained middle-aged or older individuals. This study elucidated the effects of a new long-term training stimulus on markers of muscle autophagy and unfolded protein response (UPR) and on sprint running performance in masters sprinters. Methods Thirty-two male competitive sprinters (aged 40–76 years) were randomly divided into experimental (EX) and control (CTRL) groups. The EX training program was a combination of heavy and explosive strength and sprint exercises aimed at improving sprint performance. Fifteen and thirteen participants completed the 20-week intervention period in …

Autophagosomemedicine.medical_specialtyStrength traininglihaksetPhysical Therapy Sports Therapy and RehabilitationmTORC103 medical and health sciences0302 clinical medicineSequestosome 1Internal medicineMedicineOrthopedics and Sports Medicineskeletal muscleeducationsolufysiologiaeducation.field_of_studybusiness.industryAutophagySkeletal musclemasters athleteunfolded protein response030229 sport sciencesikääntyminenEndocrinologymedicine.anatomical_structureProteostasisSprintproteiinitbusinessurheilijatMedicine & Science in Sports & Exercise
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The complex modulation of lysosomal degradation pathways by cannabinoid receptors 1 and 2

2015

The two main receptors of the endocannabinoid system, cannabinoid receptors 1 (CB1R) and 2 (CB2R), were described in the early 1990s. Since then, different physiological functions have been revealed that are linked to the activity of these two G-protein-coupled receptors. CB1R and CB2R activities influence signal cascades, which are known to play a role in the regulation of the cellular "self-digestion" process called autophagy. A variety of these signaling pathways are integrated by the mammalian target of rapamycin complex 1 (mTORC1) that acts as an inhibitor of autophagy. Others, like AMP-activated protein kinase dependent signaling pathway, are able to bypass mTORC1 to modulate the auto…

Cannabinoid receptorAutophagyContext (language use)General MedicinemTORC1BiologyEndocannabinoid systemGeneral Biochemistry Genetics and Molecular BiologyCell biologyReceptor Cannabinoid CB2Receptor Cannabinoid CB1AutophagyAnimalsHumansGeneral Pharmacology Toxicology and PharmaceuticsSignal transductionLysosomesProtein kinase AReceptorLife Sciences
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