Search results for "Aggrephagy"

showing 4 items of 4 documents

Regulation of the HTRA2 Protease Activity by an Inhibitory Antibody-Derived Peptide Ligand and the Influence on HTRA2-Specific Protein Interaction Ne…

2021

The mitochondrial serine protease HTRA2 has many versatile biological functions ranging from being an important regulator of apoptosis to being an essential component for neuronal cell survival and mitochondrial homeostasis. Loss of HTRA2 protease function is known to cause neurodegeneration, whereas overactivation of its proteolytic function is associated with cell death and inflammation. In accordance with this, our group verified in a recent study that the synthetic peptide ASGYTFTNYGLSWVR, encoding the hypervariable sequence part of an antibody, showed a high affinity for the target protein HTRA2 and triggered neuroprotection in an in vitro organ culture model for glaucoma. To unravel t…

retinaImmunoprecipitationQH301-705.5medicine.medical_treatmentMedicine (miscellaneous)PeptideAggrephagyNeuroprotectioninteraction partnersGeneral Biochemistry Genetics and Molecular BiologyArticlemedicineBiology (General)mass spectrometrychemistry.chemical_classificationProteaseHTRA2Neurodegenerationco-immunoprecipitationmedicine.diseaseProtease inhibitor (biology)Cell biologychemistryneuroprotectionTarget proteinmedicine.drugBiomedicines
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BAG3 mediates chaperone-based aggresome-targeting and selective autophagy of misfolded proteins.

2010

Increasing evidence indicates the existence of selective autophagy pathways, but the manner in which substrates are recognized and targeted to the autophagy system is poorly understood. One strategy is transport of a particular substrate to the aggresome, a perinuclear compartment with high autophagic activity. In this paper, we identify a new cellular pathway that uses the specificity of heat-shock protein 70 (Hsp70) to misfolded proteins as the basis for aggresome-targeting and autophagic degradation. This pathway is regulated by the stress-induced co-chaperone Bcl-2-associated athanogene 3 (BAG3), which interacts with the microtubule-motor dynein and selectively directs Hsp70 substrates …

Protein FoldingRecombinant Fusion ProteinsDyneinGreen Fluorescent ProteinsAggrephagyMice TransgenicBAG3BiochemistryMiceJUNQ and IPODChlorocebus aethiopsGeneticsAutophagyAnimalsHumansPoint MutationHSP70 Heat-Shock ProteinsMolecular BiologyAdaptor Proteins Signal TransducingSequence DeletionInclusion BodiesMotor NeuronsbiologySuperoxide DismutaseAutophagyScientific ReportsDyneinsTransport proteinCell biologyProtein TransportAggresomeHEK293 CellsSpinal CordChaperone (protein)COS Cellsbiology.proteinApoptosis Regulatory ProteinsProteasome InhibitorsEMBO reports
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The Role of the Multifunctional BAG3 Protein in Cellular Protein Quality Control and in Disease

2017

In neurons, but also in all other cells the complex proteostasis network is monitored and tightly regulated by the cellular protein quality control (PQC) system. Beyond folding of newly synthesized polypeptides and their refolding upon misfolding the PQC also manages the disposal of aberrant proteins either by the ubiquitin-proteasome machinery or by the autophagic-lysosomal system. Aggregated proteins are primarily degraded by a process termed selective macroautophagy (or aggrephagy). One such recently discovered selective macroautophagy pathway is mediated by the multifunctional HSP70 co-chaperone BAG3 (BCL-2-associated athanogene 3). Under acute stress and during cellular aging, BAG3 in …

0301 basic medicineHuntingtinSOD1AggrephagyReviewBAG3lcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceUbiquitinselective macroautophagymedicineprotein quality controllcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyproteostasisbiologyBAG3NeurodegenerationAutophagymedicine.diseaseCell biology030104 developmental biologyProteostasisneurodegenerative disordersbiology.proteinNeuroscienceFrontiers in Molecular Neuroscience
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Ubiquitin-independent function of optineurin in autophagic clearance of protein aggregates.

2013

Summary Aggregation of misfolded proteins and the associated loss of neurons are considered a hallmark of numerous neurodegenerative diseases. Optineurin is present in protein inclusions observed in various neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), Huntington's disease, Alzheimer's disease, Parkinson's disease, Creutzfeld-Jacob disease and Pick's disease. Optineurin deletion mutations have also been described in ALS patients. However, the role of optineurin in mechanisms of protein aggregation remains unclear. In this report, we demonstrate that optineurin recognizes various protein aggregates via its C-terminal coiled-coil domain in a ubiquitin-independent m…

HuntingtinSOD1AggrephagyCell Cycle ProteinsMice TransgenicProtein aggregationBiologyArticle03 medical and health sciencesMice0302 clinical medicineTANK-binding kinase 1UbiquitinTranscription Factor TFIIIAAutophagyAnimalsHumansPhosphorylationZebrafishZebrafish030304 developmental biologyOptineurin0303 health sciencesUbiquitinamyotrophic lateral sclerosis; Huntington disease; Huntingtin; optineurin; phosphorylation; SOD1; TBK1; ubiquitinMembrane Transport ProteinsNeurodegenerative DiseasesCell Biologybiology.organism_classification3. Good healthMice Inbred C57BLDisease Models AnimalCancer researchbiology.protein030217 neurology & neurosurgeryHeLa CellsProtein BindingJournal of cell science
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