Amyloid-like Aggregates Sequester Numerous Metastable Proteins with Essential Cellular Functions

[1]  Christopher M. Dobson,et al.  The Non-Core Regions of Human Lysozyme Amyloid Fibrils Influence Cytotoxicity , 2010, Journal of molecular biology.

[2]  C. Dobson,et al.  ANS binding reveals common features of cytotoxic amyloid species. , 2010, ACS chemical biology.

[3]  David Eisenberg,et al.  Identifying the amylome, proteins capable of forming amyloid-like fibrils , 2010, Proceedings of the National Academy of Sciences.

[4]  Fabrizio Chiti,et al.  A causative link between the structure of aberrant protein oligomers and their toxicity. , 2010, Nature chemical biology.

[5]  David T. Jones,et al.  Modularity of intrinsic disorder in the human proteome , 2010, Proteins.

[6]  A. M. Erkine,et al.  Functional interplay between chromatin remodeling complexes RSC, SWI/SNF and ISWI in regulation of yeast heat shock genes , 2009, Nucleic acids research.

[7]  Debashis Mukhopadhyay,et al.  The Role of Intrinsically Unstructured Proteins in Neurodegenerative Diseases , 2009, PloS one.

[8]  Sandhya Rani,et al.  Human Protein Reference Database—2009 update , 2008, Nucleic Acids Res..

[9]  M. Bolognesi,et al.  Function and Structure of Inherently Disordered Proteins This Review Comes from a Themed Issue on Proteins Edited Prediction of Non-folding Proteins and Regions Frequency of Disordered Regions Protein Evolution Partitioning Unstructured Proteins and Regions into Groups Involvement of Inherently Diso , 2022 .

[10]  M. Mann,et al.  MaxQuant enables high peptide identification rates, individualized p.p.b.-range mass accuracies and proteome-wide protein quantification , 2008, Nature Biotechnology.

[11]  Michele Vendruscolo,et al.  Prediction of aggregation-prone regions in structured proteins. , 2008, Journal of molecular biology.

[12]  R. Morimoto,et al.  Proteotoxic stress and inducible chaperone networks in neurodegenerative disease and aging. , 2008, Genes & development.

[13]  Richard I. Morimoto,et al.  Adapting Proteostasis for Disease Intervention , 2008, Science.

[14]  Christian Haass,et al.  The two faces of protein misfolding: gain‐ and loss‐of‐function in neurodegenerative diseases , 2008, The EMBO journal.

[15]  Sheena E. Radford,et al.  Folding versus aggregation: Polypeptide conformations on competing pathways , 2008, Archives of biochemistry and biophysics.

[16]  Judith A. Blake,et al.  The Mouse Genome Database (MGD): mouse biology and model systems , 2007, Nucleic Acids Res..

[17]  Michele Vendruscolo,et al.  Prediction of local structural stabilities of proteins from their amino acid sequences. , 2007, Structure.

[18]  M. Mann,et al.  A practical recipe for stable isotope labeling by amino acids in cell culture (SILAC) , 2006, Nature Protocols.

[19]  Janghoo Lim,et al.  ATAXIN-1 Interacts with the Repressor Capicua in Its Native Complex to Cause SCA1 Neuropathology , 2006, Cell.

[20]  Dong Jin Kim,et al.  A high-throughput screen for compounds that inhibit aggregation of the Alzheimer's peptide. , 2006, ACS chemical biology.

[21]  A. Linstedt.  Faculty Opinions recommendation of Alpha-synuclein blocks ER-Golgi traffic and Rab1 rescues neuron loss in Parkinson's models. , 2006 .

[22]  S. Lindquist,et al.  α-Synuclein Blocks ER-Golgi Traffic and Rab1 Rescues Neuron Loss in Parkinson's Models , 2006, Science.

[23]  Lilia M. Iakoucheva,et al.  Intrinsic Disorder Is a Common Feature of Hub Proteins from Four Eukaryotic Interactomes , 2006, PLoS Comput. Biol..

[24]  C. Dobson,et al.  Protein misfolding, functional amyloid, and human disease. , 2006, Annual review of biochemistry.

[25]  I. Mook‐Jung,et al.  Cytosolic amyloid-β peptide 42 escaping from degradation induces cell death , 2006 .

[26]  P. Lansbury,et al.  Are amyloid diseases caused by protein aggregates that mimic bacterial pore-forming toxins? , 2006, Quarterly Reviews of Biophysics.

[27]  Richard I. Morimoto,et al.  Progressive Disruption of Cellular Protein Folding in Models of Polyglutamine Diseases , 2006, Science.

[28]  I. Mook‐Jung,et al.  Cytosolic amyloid-beta peptide 42 escaping from degradation induces cell death. , 2006, Biochemical and biophysical research communications.

[29]  Brian J Bacskai,et al.  In vivo optical imaging of amyloid aggregates in brain: design of fluorescent markers. , 2005, Angewandte Chemie.

[30]  Zsuzsanna Dosztányi,et al.  IUPred: web server for the prediction of intrinsically unstructured regions of proteins based on estimated energy content , 2005, Bioinform..

[31]  M. Fändrich,et al.  FTIR reveals structural differences between native β‐sheet proteins and amyloid fibrils , 2004, Protein science : a publication of the Protein Society.

[32]  S. Akira,et al.  Species-Specific Recognition of Single-Stranded RNA via Toll-like Receptor 7 and 8 , 2004, Science.

[33]  T. Gibson,et al.  Protein disorder prediction: implications for structural proteomics. , 2003, Structure.

[34]  C. Dobson,et al.  Protein aggregation and aggregate toxicity: new insights into protein folding, misfolding diseases and biological evolution , 2003, Journal of Molecular Medicine.

[35]  Carl W. Cotman,et al.  Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis , 2003, Science.

[36]  H. Engelhardt,et al.  The Core of the Tetrameric Mycobacterial Porin MspA Is an Extremely Stable β-Sheet Domain* , 2003, The Journal of Biological Chemistry.

[37]  Nicholas J. Hoogenraad,et al.  Molecular Chaperones Hsp90 and Hsp70 Deliver Preproteins to the Mitochondrial Import Receptor Tom70 , 2003, Cell.

[38]  Yinan Wei,et al.  Stably folded de novo proteins from a designed combinatorial library , 2003, Protein science : a publication of the Protein Society.

[39]  Christine Wurth,et al.  Mutations that reduce aggregation of the Alzheimer's Abeta42 peptide: an unbiased search for the sequence determinants of Abeta amyloidogenesis. , 2002, Journal of molecular biology.

[40]  A. Orth,et al.  Large-scale analysis of the human and mouse transcriptomes , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[41]  F. Hartl,et al.  Molecular Chaperones in the Cytosol: from Nascent Chain to Folded Protein , 2002, Science.

[42]  R. Kingston,et al.  Transcriptional Activation Domains of Human Heat Shock Factor 1 Recruit Human SWI/SNF , 2001, Molecular and Cellular Biology.

[43]  S. Younkin,et al.  The 'Arctic' APP mutation (E693G) causes Alzheimer's disease by enhanced Aβ protofibril formation , 2001, Nature Neuroscience.

[44]  A. Barabasi,et al.  Lethality and centrality in protein networks , 2001, Nature.

[45]  R. Kopito,et al.  Impairment of the ubiquitin-proteasome system by protein aggregation. , 2001, Science.

[46]  J. Frydman.  Folding of newly translated proteins in vivo: the role of molecular chaperones. , 2001, Annual review of biochemistry.

[47]  M. Hecht,et al.  De novo amyloid proteins from designed combinatorial libraries. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[48]  M. Shearman,et al.  Toxicity of protein aggregates in PC12 cells: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. , 1999, Methods in enzymology.

[49]  S. Prusiner,et al.  Scrapie prions selectively modify the stress response in neuroblastoma cells. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[50]  T. Mcclanahan,et al.  E1a transactivation of the human HSP70 promoter is mediated through the basal transcriptional complex , 1989, Molecular and cellular biology.

[51]  R. Doolittle,et al.  A simple method for displaying the hydropathic character of a protein. , 1982, Journal of molecular biology.