Parkin promotes proteasomal degradation of p62: implication of selective vulnerability of neuronal cells in the pathogenesis of Parkinson’s disease

[1]  J. Burman,et al.  The ubiquitin kinase PINK1 recruits autophagy receptors to induce mitophagy , 2015, Nature.

[2]  Quan Chen,et al.  Mitochondrial outer-membrane E3 ligase MUL1 ubiquitinates ULK1 and regulates selenite-induced mitophagy , 2015, Autophagy.

[3]  R. Youle,et al.  The Roles of PINK1, Parkin, and Mitochondrial Fidelity in Parkinson’s Disease , 2015, Neuron.

[4]  D. Kirkpatrick,et al.  The mitochondrial deubiquitinase USP30 opposes parkin-mediated mitophagy , 2014, Nature.

[5]  T. Hirokawa,et al.  Ubiquitin is phosphorylated by PINK1 to activate parkin , 2014, Nature.

[6]  Soojay Banerjee,et al.  PINK1 phosphorylates ubiquitin to activate Parkin E3 ubiquitin ligase activity , 2014, The Journal of cell biology.

[7]  K. Hofmann,et al.  Parkin is activated by PINK1-dependent phosphorylation of ubiquitin at Ser65 , 2014, The Biochemical journal.

[8]  J. Hardy,et al.  The Parkinson’s disease genes Fbxo7 and Parkin interact to mediate mitophagy , 2013, Nature Neuroscience.

[9]  G. Dorn,et al.  PINK1-Phosphorylated Mitofusin 2 Is a Parkin Receptor for Culling Damaged Mitochondria , 2013, Science.

[10]  M. Martínez-Vicente,et al.  Brain region- and age-dependent dysregulation of p62 and NBR1 in a mouse model of Huntington's disease , 2013, Neurobiology of Disease.

[11]  Steven P. Gygi,et al.  Landscape of the PARKIN-dependent ubiquitylome in response to mitochondrial depolarization , 2013, Nature.

[12]  Michael Lazarou,et al.  PINK1 drives Parkin self-association and HECT-like E3 activity upstream of mitochondrial binding , 2013, The Journal of cell biology.

[13]  P. S. St George-Hyslop,et al.  SQSTM1 mutations in frontotemporal lobar degeneration and amyotrophic lateral sclerosis , 2012, Neurology.

[14]  M. LaVoie,et al.  The ubiquitin E3 ligase parkin regulates the proapoptotic function of Bax , 2012, Proceedings of the National Academy of Sciences.

[15]  R. Xavier,et al.  Autophagy Suppresses Interleukin-1β (IL-1β) Signaling by Activation of p62 Degradation via Lysosomal and Proteasomal Pathways* , 2011, The Journal of Biological Chemistry.

[16]  S. Ajroud‐Driss,et al.  SQSTM1 mutations in familial and sporadic amyotrophic lateral sclerosis. , 2011, Archives of neurology.

[17]  Xinnan Wang,et al.  PINK1 and Parkin Target Miro for Phosphorylation and Degradation to Arrest Mitochondrial Motility , 2011, Cell.

[18]  F. Sterky,et al.  Impaired mitochondrial transport and Parkin-independent degeneration of respiratory chain-deficient dopamine neurons in vivo , 2011, Proceedings of the National Academy of Sciences.

[19]  I. Nezis,et al.  p62, Ref(2)P and ubiquitinated proteins are conserved markers of neuronal aging, aggregate formation and progressive autophagic defects , 2011, Autophagy.

[20]  T. Dawson,et al.  PARIS (ZNF746) Repression of PGC-1α Contributes to Neurodegeneration in Parkinson's Disease , 2011, Cell.

[21]  C. Chu,et al.  Bioenergetics of neurons inhibit the translocation response of Parkin following rapid mitochondrial depolarization. , 2011, Human molecular genetics.

[22]  Min Liu,et al.  Parkin Ubiquitinates Drp1 for Proteasome-dependent Degradation , 2011, The Journal of Biological Chemistry.

[23]  A. Schapira,et al.  PINK1-parkin-dependent mitophagy involves ubiquitination of mitofusins 1 and 2: Implications for Parkinson disease pathogenesis , 2011, Autophagy.

[24]  Lei Du,et al.  Parkin ubiquitinates Drp1 for proteasome-dependent degradation: implication of dysregulated mitochondrial dynamics in Parkinson’s disease , 2011 .

[25]  R. Youle,et al.  Proteasome and p97 mediate mitophagy and degradation of mitofusins induced by Parkin , 2010, The Journal of cell biology.

[26]  A. Schapira,et al.  Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy. , 2010, Human molecular genetics.

[27]  M. Komatsu,et al.  Selective degradation of p62 by autophagy , 2010, Seminars in Immunopathology.

[28]  M. McMahon,et al.  p62/SQSTM1 Is a Target Gene for Transcription Factor NRF2 and Creates a Positive Feedback Loop by Inducing Antioxidant Response Element-driven Gene Transcription* , 2010, The Journal of Biological Chemistry.

[29]  N. Hattori,et al.  PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy , 2010, The Journal of cell biology.

[30]  M. Komatsu,et al.  Physiological significance of selective degradation of p62 by autophagy , 2010, FEBS letters.

[31]  T. Dawson,et al.  The role of parkin in familial and sporadic Parkinson's disease , 2010, Movement disorders : official journal of the Movement Disorder Society.

[32]  G. Bjørkøy,et al.  Nucleocytoplasmic Shuttling of p62/SQSTM1 and Its Role in Recruitment of Nuclear Polyubiquitinated Proteins to Promyelocytic Leukemia Bodies* , 2009, The Journal of Biological Chemistry.

[33]  Ivan Dikic,et al.  A role for ubiquitin in selective autophagy. , 2009, Molecular cell.

[34]  A. Brice,et al.  Parkinson's disease: from monogenic forms to genetic susceptibility factors. , 2009, Human molecular genetics.

[35]  Han Li,et al.  Protein degradation in Parkinson disease revisited: it's complex. , 2009, The Journal of clinical investigation.

[36]  R. Youle,et al.  Parkin is recruited selectively to impaired mitochondria and promotes their autophagy , 2008, The Journal of cell biology.

[37]  Saskia Biskup,et al.  Genes associated with Parkinson syndrome , 2008, Journal of Neurology.

[38]  Junmin Peng,et al.  Essential Role of Sequestosome 1/p62 in Regulating Accumulation of Lys63-ubiquitinated Proteins* , 2008, Journal of Biological Chemistry.

[39]  E. Masliah,et al.  alpha-Synuclein aggregates interfere with Parkin solubility and distribution: role in the pathogenesis of Parkinson disease. , 2008, The Journal of biological chemistry.

[40]  R. Szargel,et al.  Monoubiquitylation of α-Synuclein by Seven in Absentia Homolog (SIAH) Promotes Its Aggregation in Dopaminergic Cells* , 2008, Journal of Biological Chemistry.

[41]  Masaaki Komatsu,et al.  Homeostatic Levels of p62 Control Cytoplasmic Inclusion Body Formation in Autophagy-Deficient Mice , 2007, Cell.

[42]  L. Chin,et al.  Ubiquitination of α-synuclein by Siah-1 promotes α-synuclein aggregation and apoptotic cell death , 2007 .

[43]  M. LaVoie,et al.  The effects of oxidative stress on parkin and other E3 ligases , 2007, Journal of neurochemistry.

[44]  G. Bjørkøy,et al.  p62/SQSTM1 Binds Directly to Atg8/LC3 to Facilitate Degradation of Ubiquitinated Protein Aggregates by Autophagy* , 2007, Journal of Biological Chemistry.

[45]  T. Dawson.  Unraveling the role of defective genes in Parkinson's disease. , 2007, Parkinsonism & related disorders.

[46]  T. Dawson,et al.  Identification of Far Upstream Element-binding Protein-1 as an Authentic Parkin Substrate* , 2006, Journal of Biological Chemistry.

[47]  G. Bjørkøy,et al.  p62/SQSTM1: A Missing Link between Protein Aggregates and the Autophagy Machinery , 2006, Autophagy.

[48]  M. Farrer.  Genetics of Parkinson disease: paradigm shifts and future prospects , 2006, Nature Reviews Genetics.

[49]  Houeto Jean-Luc.  [Parkinson's disease]. , 2022, La Revue du praticien.

[50]  R. Palmiter,et al.  Parkin-deficient mice are not more sensitive to 6-hydroxydopamine or methamphetamine neurotoxicity , 2005, BMC Neuroscience.

[51]  D. Selkoe,et al.  Dopamine covalently modifies and functionally inactivates parkin , 2005, Nature Medicine.

[52]  K. Lim,et al.  Familial-associated mutations differentially disrupt the solubility, localization, binding and ubiquitination properties of parkin. , 2005, Human molecular genetics.

[53]  M. W. Wooten,et al.  Sequestosome 1/p62 shuttles polyubiquitinated tau for proteasomal degradation , 2005, Journal of neurochemistry.

[54]  R. Palmiter,et al.  Parkin-deficient mice are not a robust model of parkinsonism. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[55]  N. Krishna,et al.  Sequestosome 1/p62 Is a Polyubiquitin Chain Binding Protein Involved in Ubiquitin Proteasome Degradation , 2004, Molecular and Cellular Biology.

[56]  S. Lipton,et al.  Molecular pathways to neurodegeneration , 2004, Nature Medicine.

[57]  C. Haass,et al.  How does parkin ligate ubiquitin to Parkinson's disease? , 2004, EMBO reports.

[58]  K. Nakashima,et al.  Transcriptional activation of p62/A170/ZIP during the formation of the aggregates: possible mechanisms and the role in Lewy body formation in Parkinson's disease , 2004, Brain Research.

[59]  J. Troncoso,et al.  S-Nitrosylation of Parkin Regulates Ubiquitination and Compromises Parkin's Protective Function , 2004, Science.

[60]  Bryan L Roth,et al.  Parkin-deficient Mice Exhibit Nigrostriatal Deficits but Not Loss of Dopaminergic Neurons* , 2003, Journal of Biological Chemistry.

[61]  Janel O. Johnson,et al.  α-Synuclein Locus Triplication Causes Parkinson's Disease , 2003, Science.

[62]  T. Dawson,et al.  Molecular Pathways of Neurodegeneration in Parkinson's Disease , 2003, Science.

[63]  Santiago Canals,et al.  Parkin gene inactivation alters behaviour and dopamine neurotransmission in the mouse. , 2003, Human molecular genetics.

[64]  A. Singleton,et al.  alpha-Synuclein locus triplication causes Parkinson's disease. , 2003, Science.

[65]  Kurt Zatloukal,et al.  p62 Is a common component of cytoplasmic inclusions in protein aggregation diseases. , 2002, The American journal of pathology.

[66]  S. Minoshima,et al.  Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism , 1998, Nature.

[67]  M. L. Schmidt,et al.  α-Synuclein in Lewy bodies , 1997, Nature.

[68]  A. Ishikawa,et al.  Clinical analysis of 17 patients in 12 Japanese families with autosomal-recessive type juvenile parkinsonism , 1996, Neurology.