Search results for "LC3A"

showing 3 items of 3 documents

Autophagy interferes with human cytomegalovirus genome replication, morphogenesis, and progeny release.

2020

Viral infections are often accompanied by the induction of autophagy as an intrinsic cellular defense mechanism. Herpesviruses have developed strategies to evade autophagic degradation and to manipulate autophagy of the host cells to their benefit. Here we addressed the role of macroautophagy/autophagy in human cytomegalovirus replication and for particle morphogenesis. We found that proteins of the autophagy machinery localize to cytoplasmic viral assembly compartments and enveloped virions in the cytoplasm. Surprisingly, the autophagy receptor SQSTM1/p62 was also found to colocalize with HCMV capsids in the nucleus of infected cells. This finding indicates that the autophagy machinery int…

0301 basic medicineHuman cytomegalovirusCytoplasmEpstein-Barr Virus InfectionsvirusesCytomegalovirusBiology03 medical and health sciencesMultiplicity of infectionmedicineXenophagyAutophagyMorphogenesisHumansMolecular BiologyCytopathic effect030102 biochemistry & molecular biologyAutophagyCell BiologyBECN1biochemical phenomena metabolism and nutritionFibroblastsmedicine.diseaseVirus ReleaseCell biology030104 developmental biologyCytomegalovirus InfectionsMAP1LC3AResearch PaperAutophagy
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Lung autophagic response following exposure of mice to whole body irradiation, with and without amifostine

2010

Research highlights: {yields} We investigated the effect 6 Gy of WBI on the autophagic machinery of normal mouse lung. {yields} Irradiation induces dysfunction of the autophagic machinery in normal lung, characterized by decreased transcription of the LC3A/Beclin-1 mRNA and accumulation of the LC3A, and p62 proteins. {yields} The membrane bound LC3A-II protein levels increased in the cytosolic fraction (not in the pellet), contrasting the patterns noted after starvation-induced autophagy. {yields} Administration of amifostine, reversed all the LC3A and p62 findings, suggesting protection of the normal autophagic function. -- Abstract: Purpose: The effect of ionizing irradiation on the autop…

MaleAutophagosomemedicine.medical_specialtyATG8BiophysicsRadiation-Protective AgentsBiologyBiochemistryMiceAmifostineInternal medicineAutophagymedicineAnimalsta315LungMolecular BiologyRegulation of gene expressionMice Inbred BALB CMessenger RNAAutophagyCell BiologyAmifostineBlotEndocrinologyBiochemistryGamma RaysStarvationBeclin-1Apoptosis Regulatory ProteinsMicrotubule-Associated ProteinsTranscription Factor TFIIHWhole-Body IrradiationMAP1LC3ATranscription Factorsmedicine.drugBiochemical and Biophysical Research Communications
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Novel Insights into the Cellular Localization and Regulation of the Autophagosomal Proteins LC3A, LC3B and LC3C

2020

Macroautophagy is a conserved degradative process for maintaining cellular homeostasis and plays a key role in aging and various human disorders. The microtubule-associated protein 1A/1B light chain 3B (MAP1LC3B or LC3B) is commonly analyzed as a key marker for autophagosomes and as a proxy for autophagic flux. Three paralogues of the LC3 gene exist in humans: LC3A, LC3B and LC3C. The molecular function, regulation and cellular localization of LC3A and LC3C have not been investigated frequently, even if a similar function to that described for LC3B appears likely. Here, we have selectively decapacitated LC3B by three separate strategies in primary human fibroblasts and analyzed the evoked e…

autophagysequestosome 1 (p62)LC3CATG8GABARAPGABARAPCellular homeostasisProtein lipidationsirtuin 1ArticleCell LineAntibody SpecificityHumansSirtuinsAmino Acid SequenceLC3BRNA Small InterferingLC3Alcsh:QH301-705.5PhylogenyCellular localizationCell NucleusBinding SitesbiologyChemistrySirtuin 1AutophagosomesAutophagy-Related Protein 8 FamilyGeneral MedicineFibroblastsLipidsCell biologyProtein Transportlcsh:Biology (General)Gene Knockdown TechniquesSirtuinbiology.proteinApoptosis Regulatory ProteinsMicrotubule-Associated ProteinsATG8MAP1LC3BSubcellular FractionsCells
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