Signaling, polyubiquitination, trafficking, and inclusions: sequestosome 1/p62's role in neurodegenerative disease. - Test2 - elhamkhani - TriplyDB

Signaling, polyubiquitination, trafficking, and inclusions: sequestosome 1/p62's role in neurodegenerative disease.

Signaling, polyubiquitination, trafficking, and inclusions: sequestosome 1/p62's role in neurodegenerative disease.

http://www.wikidata.org/entity/Q36626380

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Macroautophagy is defective in mucolipin-1-deficient mouse neurons p62 Targeting to the autophagosome formation site requires self-oligomerization but not LC3 binding Spartin recruits PKC-ζ via the PKC-ζ-interacting proteins ZIP1 and ZIP3 to lipid droplets Boning up on autophagy: the role of autophagy in skeletal biology Glial fibrillary acidic protein is elevated in the lysosomal storage disease classical late-infantile neuronal ceroid lipofuscinosis, but is not a component of the storage material.Ubiquitin/proteasome pathway impairment in neurodegeneration: therapeutic implications The sequestosome 1/p62 attenuates cytokine gene expression in activated macrophages by inhibiting IFN regulatory factor 8 and TNF receptor-associated factor 6/NF-kappaB activity.Differential effects of UCHL1 modulation on alpha-synuclein in PD-like models of alpha-synucleinopathy.Coaggregation of RNA-binding proteins in a model of TDP-43 proteinopathy with selective RGG motif methylation and a role for RRM1 ubiquitination Neuropathology of the Mcoln1(-/-) knockout mouse model of mucolipidosis type IV.Oxidative damage to the promoter region of SQSTM1/p62 is common to neurodegenerative disease.Recent advances in our understanding of neurodegeneration.Dynamics of the degradation of ubiquitinated proteins by proteasomes and autophagy: association with sequestosome 1/p62.Human-IAPP disrupts the autophagy/lysosomal pathway in pancreatic β-cells: protective role of p62-positive cytoplasmic inclusions Drosha inclusions are new components of dipeptide-repeat protein aggregates in FTLD-TDP and ALS C9orf72 expansion cases p62 Pathology Model in the Rat Substantia Nigra with Filamentous Inclusions and Progressive Neurodegeneration Activation of the macroautophagic system in scrapie-infected experimental animals and human genetic prion diseases Pattern of ubiquilin pathology in ALS and FTLD indicates presence of C9ORF72 hexanucleotide expansion.Ref(2)P, the Drosophila melanogaster homologue of mammalian p62, is required for the formation of protein aggregates in adult brain.How a cell deals with abnormal proteins. Pathogenetic mechanisms in protein aggregation diseases.Lysosomal membrane permeability stimulates protein aggregate formation in neurons of a lysosomal disease Autophagy-physiology and pathophysiology.Age-associated oxidative damage to the p62 promoter: implications for Alzheimer disease.Proteins that mediate protein aggregation and cytotoxicity distinguish Alzheimer's hippocampus from normal controls.Inclusion bodies enriched for p62 and polyubiquitinated proteins in macrophages protect against atherosclerosis β Cell-specific increased expression of calpastatin prevents diabetes induced by islet amyloid polypeptide toxicity.scyllo-Inositol promotes robust mutant Huntingtin protein degradation.Defining an Embedded Code for Protein Ubiquitination Implications of autophagy for glomerular aging and disease.The adaptor protein p62/SQSTM1 in osteoclast signaling pathways.Relationship between the proteasomal system and autophagy.Expression of the autophagy substrate SQSTM1/p62 is restored during prolonged starvation depending on transcriptional upregulation and autophagy-derived amino acids.A small molecule inhibitor of inducible heat shock protein 70.Parkin deficiency increases the resistance of midbrain neurons and glia to mild proteasome inhibition: the role of autophagy and glutathione homeostasis.Autophagy inhibition compromises degradation of ubiquitin-proteasome pathway substrates.CNOT2 promotes degradation of p62/SQSTM1 as a negative regulator in ATG5 dependent autophagy.Autophagy Dysregulation in ALS: When Protein Aggregates Get Out of Hand.cAMP stimulates the ubiquitin/proteasome pathway in rat spinal cord neurons.A role for sequestosome 1/p62 in mitochondrial dynamics, import and genome integrity.A bacterial pore-forming toxin forms aggregates in cells that resemble those associated with neurodegenerative diseases.

P2860

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P2860

Signaling, polyubiquitination, trafficking, and inclusions: sequestosome 1/p62's role in neurodegenerative disease.

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Signaling, polyubiquitination, ...... in neurodegenerative disease.

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Signaling, polyubiquitination, ...... in neurodegenerative disease.

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Signaling, polyubiquitination, ...... e in neurodegenerative disease

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J Ramesh Babu

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M Lamar Seibenhener

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Marie W Wooten

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Michael C Wooten

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Michael G Paine

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Xiao Hu

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P2860

Parkin suppresses unfolded protein stress-induced cell death through its E3 ubiquitin-protein ligase activity

p62 forms a ternary complex with PKCzeta and PAR-4 and antagonizes PAR-4-induced PKCzeta inhibition

Structure and functional properties of the ubiquitin binding protein p62

The ubiquitin-proteasome proteolytic pathway: destruction for the sake of construction

PAR-4 is involved in regulation of beta-secretase cleavage of the Alzheimer amyloid precursor protein

Sequestosome 1/p62 shuttles polyubiquitinated tau for proteasomal degradation

Structure of the ubiquitin-associated domain of p62 (SQSTM1) and implications for mutations that cause Paget's disease of bone

Localization of atypical protein kinase C isoforms into lysosome-targeted endosomes through interaction with p62.

IFN-gamma-induced immune adaptation of the proteasome system is an accelerated and transient response

Ataxin-3 interactions with rad23 and valosin-containing protein and its associations with ubiquitin chains and the proteasome are consistent with a role in ubiquitin-mediated proteolysis

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neurodegeneration

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