Search results for "ATG5"

showing 10 items of 11 documents

Hepatitis B Virus Subverts the Autophagy Elongation Complex Atg5-12/16L1 and Does Not Require Atg8/LC3 Lipidation for Viral Maturation

2018

ABSTRACT Previous studies indicated that hepatitis B virus (HBV) stimulates autophagy to favor its production. To understand how HBV co-opts autophagy as a proviral machinery, we studied the roles of key autophagy proteins in HBV-replicating liver cell cultures. RNA interference-mediated silencing of Atg5, Atg12, and Atg16L1, which promote autophagophore expansion and LC3 membrane conjugation, interfered with viral core/nucleocapsid (NC) formation/stability and strongly diminished virus yields. Concomitantly, the core/NC membrane association and their sorting to envelope-positive compartments were perturbed. A close inspection of the HBV/autophagy cross talk revealed that the virus depended…

0301 basic medicineHepatitis B virusATG8Autophagosome maturationImmunologyATG5Autophagy-Related ProteinsBiologymedicine.disease_causeVirus ReplicationMicrobiologyVirusAutophagy-Related Protein 5ATG1203 medical and health sciencesVirologyCell Line TumormedicineAutophagyHumansHepatitis B virusAutophagyAutophagy-Related Protein 8 FamilyHepatitis BCell biologyVirus-Cell Interactions030104 developmental biologyViral replicationInsect ScienceGene Knockdown TechniquesMultiprotein ComplexesMicrotubule-Associated ProteinsAutophagy-Related Protein 12
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Role of p62/SQSTM1 beyond autophagy: a lesson learned from drug-induced toxicity in vitro

2018

Background and Purpose SQSTM1/p62 is a multifunctional, stress-induced, scaffold protein involved in multiple cellular processes including autophagic clearance, regulation of inflammatory responses and redox homeostasis. Its altered function has been associated with different human pathologies, such as neurodegenerative, metabolic and bone diseases (down-regulation), and cancerogenesis (up-regulation). However, its role in the off-target effects of clinically used drugs is still not understood. Experimental Approach We evaluated the expression of p62 in cultured Hep3B cells and their derived ρ° cells (lacking mitochondria), along with markers of autophagy and mitochondrial dysfunction. The …

0301 basic medicinePharmacologyMitochondrial ROSScaffold proteinAutophagyATG5InflammasomePharmacologyMitochondrionBiologyCell biology03 medical and health sciences030104 developmental biologymedicineGene silencingViability assaymedicine.drugBritish Journal of Pharmacology
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BAG3 regulates total MAP1LC3B protein levels through a translational but not transcriptional mechanism

2015

Autophagy is mainly regulated by post-translational and lipid modifications of ATG proteins. In some scenarios, the induction of autophagy is accompanied by increased levels of certain ATG mRNAs such as MAP1LC3B/LC3B, ATG5 or ATG12. However, little is known about the regulation of ATG protein synthesis at the translational level. The cochaperone of the HSP70 system BAG3 (BCL2-associated athanogene 3) has been associated to LC3B lipidation through an unknown mechanism. In the present work, we studied how BAG3 controls autophagy in HeLa and HEK293 cells. Our results showed that BAG3 regulates the basal amount of total cellular LC3B protein by controlling its mRNA translation. This effect was …

0301 basic medicineProteasome Endopeptidase ComplexTranscription GeneticATG8ATG5BiologyBAG3ATG1203 medical and health sciences0302 clinical medicineProtein biosynthesisHumansRNA MessengerMolecular BiologyAdaptor Proteins Signal TransducingGeneticsGene knockdownAutophagyCell BiologyLipidsBasic Research PaperCell biologyHEK293 Cells030104 developmental biologyProtein BiosynthesisProteolysisApoptosis Regulatory ProteinsLysosomesMicrotubule-Associated ProteinsMAP1LC3B030217 neurology & neurosurgeryHeLa Cells
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Induction of Autophagy by Pterostilbene Contributes to the Prevention of Renal Fibrosis via Attenuating NLRP3 Inflammasome Activation and Epithelial-…

2020

Chronic kidney disease (CKD) is recognized as a global public health problem. NLRP3 inflammasome activation has been characterized to mediate diverse aspect mechanisms of CKD through regulation of proinflammatory cytokines, tubulointerstitial injury, glomerular diseases, renal inflammation, and fibrosis pathways. Autophagy is a characterized negative regulation mechanism in the regulation of the NLRP3 inflammasome, which is now recognized as the key regulator in the pathogenesis of inflammation and fibrosis in CKD. Thus, autophagy is undoubtedly an attractive target for developing new renal protective treatments of kidney disease via its potential effects in regulation of inflammasome. Howe…

0301 basic medicineautophagypterostilbeneATG5epithelial-mesenchymal transitionInflammationProinflammatory cytokine03 medical and health sciencesCell and Developmental Biology0302 clinical medicineFibrosismedicineRenal fibrosisEpithelial–mesenchymal transitionlcsh:QH301-705.5Original Researchbusiness.industryAutophagyInflammasomeCell Biologymedicine.diseaserenal fibrosisNLRP3 inflammasome030104 developmental biologylcsh:Biology (General)030220 oncology & carcinogenesisCancer researchmedicine.symptombusinessDevelopmental Biologymedicine.drugFrontiers in Cell and Developmental Biology
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Systemic Oxidative Stress and Visceral Adipose Tissue Mediators of NLRP3 Inflammasome and Autophagy Are Reduced in Obese Type 2 Diabetic Patients Tre…

2020

Obesity is a low-grade inflammatory condition affecting a range of individuals, from metabolically healthy obese (MHO) subjects to type 2 diabetes (T2D) patients. Metformin has been shown to display anti-inflammatory properties, though the underlying molecular mechanisms are unclear. To study whether the effects of metformin are mediated by changes in the inflammasome complex and autophagy in visceral adipose tissue (VAT) of obese patients, a biopsy of VAT was obtained from a total of 68 obese patients undergoing gastric bypass surgery. The patients were clustered into two groups: MHO patients and T2D patients treated with metformin. Patients treated with metformin showed decreased levels o…

0301 basic medicinemedicine.medical_specialtyvisceral adipose tissue (VAT)obesityautophagyendocrine system diseasesPhysiologyinflammatory cytokinesClinical BiochemistryATG5Adipose tissue030209 endocrinology & metabolismLeukocyte homeostasisType 2 diabetesBiochemistryArticleProinflammatory cytokine03 medical and health sciences0302 clinical medicineInternal medicinemedicineoxidative stressMolecular Biologytype 2 diabetes (T2D)business.industrylcsh:RM1-950nutritional and metabolic diseasesInflammasomeCell Biologymedicine.diseaseMetforminlcsh:Therapeutics. Pharmacology030104 developmental biologyEndocrinologybusinessmetforminInflammasome complexmedicine.drugAntioxidants (Basel, Switzerland)
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Evidence that autophagy, but not the unfolded protein response, regulates the expression of IL-23 in the gut of patients with ankylosing spondylitis …

2013

OBJECTIVES: Interleukin (IL)-23 has been implicated in the pathogenesis of ankylosing spondylitis (AS). The aim of the study was to clarify the mechanisms underlying the increased IL-23 expression in the gut of AS patients. METHODS: Consecutive gut biopsies from 30 HLA-B27(+) AS patients, 15 Crohn's disease (CD) patients and 10 normal subjects were obtained. Evidence for HLA-B27 misfolding was studied. Unfolded protein response (UPR) and autophagy were assessed by RT-PCR and immunohistochemistry. The contribution of UPR and autophagy in the regulation of IL-23 expression was evaluated in in vitro experiments on isolated lamina propria mononuclear cells (LPMCs). RESULTS: Intracellular coloca…

AdultMaleProtein FoldingBiopsyImmunologyATG5Gene ExpressionInflammationdigestive systemArticleGeneral Biochemistry Genetics and Molecular BiologyATG12Young AdultCrohn DiseaseRheumatologyDownregulation and upregulationSettore BIO/13 - Biologia Applicataankylosing spondylitisAutophagymedicineInterleukin 23HumansImmunology and AllergySpondylitis AnkylosingHLA-B27 AntigenAgedMucous Membranebusiness.industryAutophagyInterleukinIleitisMiddle AgedIntestinesInterleukin 23Settore MED/16 - ReumatologiaImmunologyInterleukin-23 Subunit p19Unfolded Protein ResponseUnfolded protein responseFemalemedicine.symptombusinessAnnals of the Rheumatic Diseases
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Response to: 'IL-23 expression and activation of autophagy in synovium and PBMCs of HLA-B27 positive patients with ankylosing spondylitis' by Neerinc…

2014

We read with interest the study by Neerinckx et al 1 addressing the expression of interleukin (IL)-23p19 and of autophagy genes in the synovium and in the peripheral blood mononuclear cells of patients with ankylosing spondylitis (AS). Differently from our observation in the gut,2 the authors failed to demonstrate any significant increase by RT-PCR in the expression of synovium autophagy-related genes (ATG16L1, IRGM, MAP1LC3A, ATG5, HSPA8 and HSP90AA1) together with no significant overexpression of IL-23p19 compared with disease and healthy controls. We have previously demonstrated by immunohistochemistry that in the …

Ankylosing spondylitisIL-23 Ankylosing Spondylitisbusiness.industryAnkylosing SpondylitisImmunologyATG5AutophagyInterleukinmedicine.diseasePeripheral blood mononuclear cellGeneral Biochemistry Genetics and Molecular BiologyRheumatologyIL-23ImmunologyIRGMmedicineInterleukin 23Immunology and AllergybusinessATG16L1
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Abstract 753: Genomic alterations of autophagy genes disrupts autophagic flux in human lung adenocarcinomas

2015

Abstract Targeted therapy using EGFR tyrosine kinase inhibitor (TKI) is a standard therapy for a subset of non-small cell lung cancer (NSCLC) patients with lung adenocarcinomas (LADs) harboring EGFR kinase domain mutations; however, EGFR TKI therapy shows limited efficacy due to de novo and acquired resistance. Consequently, formulating strategies to potentiate the efficacy of EGFR TKI is of great interest. In EGFR TKI sensitive cells harboring EGFR mutation, it has been shown that EGFR inhibition induces autophagy to protect the cells from metabolic stress. Hydroxychloroquine (HQ), an inhibitor of autophagy, has been shown to potentiate EGFR TKIs in preclinical models, however, preliminary…

Cancer Researchmedicine.medical_treatmentATG5AutophagyBiologyBioinformaticsmedicine.diseaseTargeted therapyOncologyProtein kinase domainChromosome 3Cancer researchmedicineErlotinibLung cancerGenemedicine.drugCancer Research
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RAB3GAP1 and RAB3GAP2 modulate basal and rapamycin-induced autophagy

2014

Macroautophagy is a degradative pathway that sequesters and transports cytosolic cargo in autophagosomes to lysosomes, and its deterioration affects intracellular proteostasis. Membrane dynamics accompanying autophagy are mostly elusive and depend on trafficking processes. RAB GTPase activating proteins (RABGAPs) are important factors for the coordination of cellular vesicle transport systems, and several TBC (TRE2-BUB2-CDC16) domain-containing RABGAPs are associated with autophagy. Employing C. elegans and human primary fibroblasts, we show that RAB3GAP1 and RAB3GAP2, which are components of the TBC domain-free RAB3GAP complex, influence protein aggregation and affect autophagy at basal an…

GTPase-activating proteinlipid dropletsrab3 GTP-Binding ProteinsATG16L1DMSO dimethyl sulfoxideFEZ20302 clinical medicineATG autophagy-relatedPhagosomesDAPI 4’ 6-diamidino-2-phenylindoleSQSTM1 sequestosome 1ATG16L1MAP1LC3 microtubule-associated protein 1 light chain 3GFP green fluorescent protein0303 health sciencesGABARAP GABA(A) receptor-associated proteinGTPase-Activating ProteinsCell biologyRAB3GAP1RAB3GAP2RABGAP RAB GTPase activating proteinATG3autophagyCALCOCO2 calcium binding and coiled-coil domain 2Basic Research PaperseV empty vectorATG8ATG5PBS phosphate-buffered salineBiologyPE phosphatidylethanolamineTBC domain TRE2-BUB2-CDC16 domainBAG3GEF guanine nucleotide exchange factor03 medical and health sciencesC. elegans Caenorhabditis elegansAnimalsHumansCaenorhabditis elegansMolecular Biology030304 developmental biologySirolimusDPH 1 6-diphenyl-1 3 5-hexatrieneproteostasisAutophagyBiological TransportCell BiologyFEZ1Bafi bafilomycin A1FEZ fasciculation and elongation protein zetaNBR1 neighbor of BRCA1 gene 1ProteostasissiRNA small interfering RNABSA bovine serum albuminRabLysosomes030217 neurology & neurosurgeryAutophagy
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SAT0378 Autophagy is Up-Regulated in the Salivary Glands of Primary Sjogren's Syndrome Patients and Correlates with the Focus Score and Disease Activ…

2015

Background Autophagy is now considered as a major regulator in trafficking events that activates innate and adaptive immunity and consistent evidence supports its role in autoimmunity (1). Primary Sjogren9s syndrome (pSS) is a systemic autoimmune disease characterized by infiltration of exocrine glands by T and B cells that, producing chemokines and cytokines, coordinate the chronic inflammatory process. No data on the role of autophagy in pSS are available in humans, although studies in mice demonstrated its involvement in the salivary and lacrimal gland homeostasis (2,3). Objectives We investigated the autophagy process in salivary gland tissue and in peripheral T lymphocytes from pSS pat…

Programmed cell deathExocrine glandPathologymedicine.medical_specialtySalivary glandbusiness.industryImmunologyAutophagyATG5medicine.disease_causeAcquired immune systemGeneral Biochemistry Genetics and Molecular BiologyAutoimmunitymedicine.anatomical_structureRheumatologySicca syndromeImmunologymedicineImmunology and AllergybusinessAnnals of the Rheumatic Diseases
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