Mutant FUS induces endoplasmic reticulum stress in amyotrophic lateral sclerosis and interacts with protein disulfide-isomerase
暂无分享,去创建一个
M. Horne | K. Williams | I. Blair | S. Warraich | A. Walker | J. Atkin | K. Soo | J. Orian | M. Farg | Hong Pham | Manal A. Farg
[1] G. Logroscino,et al. FUS mutations in sporadic amyotrophic lateral sclerosis: Clinical and genetic analysis , 2012, Neurobiology of Aging.
[2] J. Jia,et al. Nuclear localization sequence of FUS and induction of stress granules by ALS mutants , 2011, Neurobiology of Aging.
[3] R. Takahashi,et al. Protein disulfide isomerase-immunopositive inclusions in patients with amyotrophic lateral sclerosis , 2011, Amyotrophic lateral sclerosis : official publication of the World Federation of Neurology Research Group on Motor Neuron Diseases.
[4] A. Gitler,et al. Molecular Determinants and Genetic Modifiers of Aggregation and Toxicity for the ALS Disease Protein FUS/TLS , 2011, PLoS biology.
[5] C. Wessig,et al. C-terminal FUS/TLS mutations in familial and sporadic ALS in Germany , 2011, Neurobiology of Aging.
[6] Jiou Wang,et al. TDP-43 neurotoxicity and protein aggregation modulated by heat shock factor and insulin/IGF-1 signaling. , 2011, Human molecular genetics.
[7] J. Trojanowski,et al. Extensive FUS‐Immunoreactive Pathology in Juvenile Amyotrophic Lateral Sclerosis with Basophilic Inclusions , 2010, Brain pathology.
[8] Robert H. Brown,et al. Mutant FUS proteins that cause amyotrophic lateral sclerosis incorporate into stress granules. , 2010, Human molecular genetics.
[9] I. Mackenzie,et al. ALS‐associated fused in sarcoma (FUS) mutations disrupt Transportin‐mediated nuclear import , 2010, The EMBO journal.
[10] J. Lowe,et al. Juvenile ALS with basophilic inclusions is a FUS proteinopathy with FUS mutations , 2010, Neurology.
[11] A. Salminen,et al. Endoplasmic Reticulum Stress in Age-Related Macular Degeneration: Trigger for Neovascularization , 2010, Molecular medicine.
[12] Johan Jacobsson,et al. Novel Antibodies Reveal Inclusions Containing Non-Native SOD1 in Sporadic ALS Patients , 2010, PloS one.
[13] Eran Perlson,et al. Retrograde axonal transport: pathways to cell death? , 2010, Trends in Neurosciences.
[14] D. Pincus,et al. BiP Binding to the ER-Stress Sensor Ire1 Tunes the Homeostatic Behavior of the Unfolded Protein Response , 2010, PLoS biology.
[15] E. Mugnaini,et al. FUS‐immunoreactive inclusions are a common feature in sporadic and non‐SOD1 familial amyotrophic lateral sclerosis , 2010, Annals of neurology.
[16] A. Goris,et al. The occurrence of mutations in FUS in a Belgian cohort of patients with familial ALS , 2010, European journal of neurology.
[17] D. Cleveland,et al. TDP-43 and FUS/TLS: emerging roles in RNA processing and neurodegeneration. , 2010, Human molecular genetics.
[18] T. Iwaki,et al. Multiple system degeneration with basophilic inclusions in Japanese ALS patients with FUS mutation , 2010, Acta Neuropathologica.
[19] M. Kiernan,et al. FUS mutations in amyotrophic lateral sclerosis: clinical, pathological, neurophysiological and genetic analysis , 2009, Journal of Neurology, Neurosurgery & Psychiatry.
[20] N. Harel,et al. Reticulon-4A (Nogo-A) Redistributes Protein Disulfide Isomerase to Protect Mice from SOD1-Dependent Amyotrophic Lateral Sclerosis , 2009, The Journal of Neuroscience.
[21] H. Kretzschmar,et al. A new subtype of frontotemporal lobar degeneration with FUS pathology. , 2009, Brain : a journal of neurology.
[22] G. Comi,et al. Mutations of FUS gene in sporadic amyotrophic lateral sclerosis , 2009, Journal of Medical Genetics.
[23] P. Caroni,et al. A role for motoneuron subtype–selective ER stress in disease manifestations of FALS mice , 2009, Nature Neuroscience.
[24] J L Haines,et al. Supporting Online Material Materials and Methods Figs. S1 to S7 Tables S1 to S4 References Mutations in the Fus/tls Gene on Chromosome 16 Cause Familial Amyotrophic Lateral Sclerosis , 2022 .
[25] Xun Hu,et al. Mutations in FUS, an RNA Processing Protein, Cause Familial Amyotrophic Lateral Sclerosis Type 6 , 2009, Science.
[26] Feng Ding,et al. Dynamical roles of metal ions and the disulfide bond in Cu, Zn superoxide dismutase folding and aggregation , 2008, Proceedings of the National Academy of Sciences.
[27] A. Ståhlberg,et al. The multifunctional FUS, EWS and TAF15 proto-oncoproteins show cell type-specific expression patterns and involvement in cell spreading and stress response , 2008, BMC Cell Biology.
[28] A. Grierson,et al. Role of axonal transport in neurodegenerative diseases. , 2008, Annual review of neuroscience.
[29] Anthony W. Zoghbi,et al. The Amyotrophic Lateral Sclerosis 8 Protein VAPB Is Cleaved, Secreted, and Acts as a Ligand for Eph Receptors , 2008, Cell.
[30] M. Horne,et al. RETRACTED: Endoplasmic reticulum stress and induction of the unfolded protein response in human sporadic amyotrophic lateral sclerosis , 2008, Neurobiology of Disease.
[31] M. Schröder. Endoplasmic reticulum stress responses , 2008, Cellular and Molecular Life Sciences.
[32] M. Portero-Otín,et al. Oxidative and endoplasmic reticulum stress interplay in sporadic amyotrophic lateral sclerosis. , 2007, Brain : a journal of neurology.
[33] Y. Itoyama,et al. An In Vitro Model for Lewy Body-Like Hyaline Inclusion/Astrocytic Hyaline Inclusion: Induction by ER Stress with an ALS-Linked SOD1 Mutation , 2007, PloS one.
[34] G. Sobue,et al. Disulfide Bond Mediates Aggregation, Toxicity, and Ubiquitylation of Familial Amyotrophic Lateral Sclerosis-linked Mutant SOD1* , 2007, Journal of Biological Chemistry.
[35] Tetsuro Ito,et al. Vaticanol B, a resveratrol tetramer, regulates endoplasmic reticulum stress and inflammation. , 2007, American journal of physiology. Cell physiology.
[36] Kozo Kaibuchi,et al. Molecular Mechanisms of Axon Specification and Neuronal Disorders , 2006, Annals of the New York Academy of Sciences.
[37] P. Hart. Pathogenic superoxide dismutase structure, folding, aggregation and turnover. , 2006, Current opinion in chemical biology.
[38] D. Borchelt,et al. Mapping superoxide dismutase 1 domains of non‐native interaction: roles of intra‐ and intermolecular disulfide bonding in aggregation , 2006, Journal of neurochemistry.
[39] R. Kaufman,et al. ER stress signaling by regulated splicing: IRE1/HAC1/XBP1. , 2005, Methods.
[40] R. Kaufman,et al. ER stress and the unfolded protein response. , 2005, Mutation research.
[41] A. Cooper,et al. Degradation of misfolded proteins prevents ER-derived oxidative stress and cell death. , 2004, Molecular cell.
[42] Nobutaka Hirokawa,et al. Kinesin Transports RNA Isolation and Characterization of an RNA-Transporting Granule , 2004, Neuron.
[43] H. Gilbert,et al. Protein disulfide isomerase. , 2004, Biochimica et biophysica acta.
[44] M. Tohyama,et al. Apoptosis induced by endoplasmic reticulum stress depends on activation of caspase-3 via caspase-12 , 2004, Neuroscience Letters.
[45] Jeffrey D. Rothstein,et al. From charcot to lou gehrig: deciphering selective motor neuron death in als , 2001, Nature Reviews Neuroscience.
[46] F. Urano,et al. Coupling of stress in the ER to activation of JNK protein kinases by transmembrane protein kinase IRE1. , 2000, Science.
[47] D. Immanuel,et al. TLS (FUS) binds RNA in vivo and engages in nucleo-cytoplasmic shuttling. , 1997, Journal of cell science.
[48] M. Tuite,et al. Protein disulphide isomerase: building bridges in protein folding. , 1994, Trends in biochemical sciences.
[49] H. Gilbert,et al. Protein disulfide isomerase exhibits chaperone and anti-chaperone activity in the oxidative refolding of lysozyme. , 1994, The Journal of biological chemistry.
[50] J. Aten,et al. Measurement of co‐localization of objects in dual‐colour confocal images , 1993, Journal of microscopy.
[51] M. Horne,et al. Protein disulphide isomerase protects against protein aggregation and is S-nitrosylated in amyotrophic lateral sclerosis. , 2010, Brain : a journal of neurology.
[52] M. Miura,et al. A transgenic mouse model for monitoring endoplasmic reticulum stress , 2004, Nature Medicine.