CoChat
Sign Up
Cited by 76

The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.

Mitochondria and endoplasmic reticulum crosstalk in amyotrophic lateral sclerosis

Manfredi, Giovanni, Kawamata, Hibiki·2016·Neurobiology of Disease
DOI 10.1016/j.nbd.2015.08.004PMC PMC4754163
Open this paper in CoChat — free account

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1016/j.nbd.2015.08.004

Cites

8 of 8 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Research works printed but not linked: 116

  1. Abramzon, 2012, Valosin-containing protein (VCP) mutations in sporadic amyotrophic lateral sclerosis, Neurobiol. Aging, 33, 10.1016/j.neurobiolaging.2012.04.005 · DOI
  2. Ahtoniemi, 2008, Mutant SOD1 from spinal cord of G93A rats is destabilized and binds to inner mitochondrial membrane, Neurobiol. Dis., 32, 479, 10.1016/j.nbd.2008.08.010 · DOI
  3. Ajroud-Driss, 2015, Mutation in the novel nuclear-encoded mitochondrial protein CHCHD10 in a family with autosomal dominant mitochondrial myopathy, Neurogenetics, 16, 1, 10.1007/s10048-014-0421-1 · DOI
  4. Albers, 2000, Mitochondrial dysfunction and oxidative stress in aging and neurodegenerative disease, J. Neural Transm. Suppl., 59, 133
  5. Al-Saif, 2011, A mutation in sigma-1 receptor causes juvenile amyotrophic lateral sclerosis, Ann. Neurol., 70, 913, 10.1002/ana.22534 · DOI
  6. Arruda, 2014, Chronic enrichment of hepatic endoplasmic reticulum-mitochondria contact leads to mitochondrial dysfunction in obesity, Nat. Med., 20, 1427, 10.1038/nm.3735 · DOI
  7. Atkin, 2006, Induction of the unfolded protein response in familial amyotrophic lateral sclerosis and association of protein-disulfide isomerase with superoxide dismutase 1, J. Biol. Chem., 281, 30152, 10.1074/jbc.M603393200 · DOI
  8. Atkin, 2008, Endoplasmic reticulum stress and induction of the unfolded protein response in human sporadic amyotrophic lateral sclerosis, Neurobiol. Dis., 30, 400, 10.1016/j.nbd.2008.02.009 · DOI · Paper page
  9. Bannwarth, 2014, A mitochondrial origin for frontotemporal dementia and amyotrophic lateral sclerosis through CHCHD10 involvement, Brain, 137, 2329, 10.1093/brain/awu138 · DOI
  10. Barbara, 2002, IP3-dependent calcium-induced calcium release mediates bidirectional calcium waves in neurones: functional implications for synaptic plasticity, Biochim. Biophys. Acta, 1600, 12, 10.1016/S1570-9639(02)00439-9 · DOI
  11. Baughman, 2011, Integrative genomics identifies MCU as an essential component of the mitochondrial calcium uniporter, Nature, 476, 341, 10.1038/nature10234 · DOI
  12. Bernard-Marissal, 2012, Reduced calreticulin levels link endoplasmic reticulum stress and Fas-triggered cell death in motoneurons vulnerable to ALS, J. Neurosci., 32, 4901, 10.1523/JNEUROSCI.5431-11.2012 · DOI
  13. Bernard-Marissal, 2015, Dysfunction in endoplasmic reticulum-mitochondria crosstalk underlies SIGMAR1 loss of function mediated motor neuron degeneration, Brain, 138, 875, 10.1093/brain/awv008 · DOI · Paper page
  14. Bockler, 2014, ER-mitochondria contacts as sites of mitophagosome formation, Autophagy, 10, 1346, 10.4161/auto.28981 · DOI
  15. Bockler, 2014, Mitochondrial ER contacts are crucial for mitophagy in yeast, Dev. Cell, 28, 450, 10.1016/j.devcel.2014.01.012 · DOI
  16. Bogdanov, 1998, Elevated “hydroxyl radical” generation in vivo in an animal model of amyotrophic lateral sclerosis, J. Neurochem., 71, 1321, 10.1046/j.1471-4159.1998.71031321.x · DOI
  17. Borchelt, 1994, Superoxide dismutase 1 with mutations linked to familial amyotrophic lateral sclerosis possesses significant activity, Proc. Natl. Acad. Sci. U. S. A., 91, 8292, 10.1073/pnas.91.17.8292 · DOI
  18. Bravo, 2011, Increased ER-mitochondrial coupling promotes mitochondrial respiration and bioenergetics during early phases of ER stress, J. Cell Sci., 124, 2143, 10.1242/jcs.080762 · DOI
  19. Cardenas, 2010, Essential regulation of cell bioenergetics by constitutive InsP3 receptor Ca2+ transfer to mitochondria, Cell, 142, 270, 10.1016/j.cell.2010.06.007 · DOI · Paper page
  20. Carri, 2015, Oxidative stress and mitochondrial damage: importance in non-SOD1 ALS, Front. Cell. Neurosci., 9, 41
  21. Chiang, 2012, In vivo tagging and characterization of S-glutathionylated proteins by a chemoenzymatic method, Angew. Chem. Int. Ed. Engl., 51, 5871, 10.1002/anie.201200321 · DOI
  22. Cho, 2009, S-nitrosylation of Drp1 mediates beta-amyloid-related mitochondrial fission and neuronal injury, Science, 324, 102, 10.1126/science.1171091 · DOI · Paper page
  23. Cozzolino, 2012, Mitochondrial dysfunction in ALS, Prog. Neurobiol., 97, 54, 10.1016/j.pneurobio.2011.06.003 · DOI
  24. Csordas, 2006, Structural and functional features and significance of the physical linkage between ER and mitochondria, J. Cell Biol., 174, 915, 10.1083/jcb.200604016 · DOI
  25. Cutler, 2002, Evidence that accumulation of ceramides and cholesterol esters mediates oxidative stress-induced death of motor neurons in amyotrophic lateral sclerosis, Ann. Neurol., 52, 448, 10.1002/ana.10312 · DOI
  26. Damiano, 2006, Neural mitochondrial Ca2+ capacity impairment precedes the onset of motor symptoms in G93A Cu/Zn-superoxide dismutase mutant mice, J. Neurochem., 96, 1349, 10.1111/j.1471-4159.2006.03619.x · DOI
  27. De Stefani, 2011, A forty-kilodalton protein of the inner membrane is the mitochondrial calcium uniporter, Nature, 476, 336, 10.1038/nature10230 · DOI
  28. De Vos, 2012, VAPB interacts with the mitochondrial protein PTPIP51 to regulate calcium homeostasis, Hum. Mol. Genet., 21, 1299, 10.1093/hmg/ddr559 · DOI
  29. Eckenrode, 2010, Apoptosis protection by Mcl-1 and Bcl-2 modulation of inositol 1,4,5-trisphosphate receptor-dependent Ca2+ signaling, J. Biol. Chem., 285, 13678, 10.1074/jbc.M109.096040 · DOI
  30. Estevez, 1998, Role of endogenous nitric oxide and peroxynitrite formation in the survival and death of motor neurons in culture, Prog. Brain Res., 118, 269, 10.1016/S0079-6123(08)63214-8 · DOI
  31. Farg, 2012, Mutant FUS induces endoplasmic reticulum stress in amyotrophic lateral sclerosis and interacts with protein disulfide-isomerase, Neurobiol. Aging, 33, 2855, 10.1016/j.neurobiolaging.2012.02.009 · DOI
  32. Fernandez-Santiago, 2011, No evidence of association of FLJ10986 and ITPR2 with ALS in a large German cohort, Neurobiol. Aging, 32, e1
  33. Ferrante, 1997, Evidence of increased oxidative damage in both sporadic and familial amyotrophic lateral sclerosis, J. Neurochem., 69, 2064, 10.1046/j.1471-4159.1997.69052064.x · DOI
  34. Filezac de L'Etang, 2015, Marinesco–Sjogren syndrome protein SIL1 regulates motor neuron subtype-selective ER stress in ALS, Nat. Neurosci., 18, 227, 10.1038/nn.3903 · DOI
  35. Forrest, 2013, Increased levels of phosphoinositides cause neurodegeneration in a Drosophila model of amyotrophic lateral sclerosis, Hum. Mol. Genet., 22, 2689, 10.1093/hmg/ddt118 · DOI
  36. Fujimoto, 2012, The role of cholesterol in the association of endoplasmic reticulum membranes with mitochondria, Biochem. Biophys. Res. Commun., 417, 635, 10.1016/j.bbrc.2011.12.022 · DOI · Paper page
  37. Fukunaga, 2015, The role of SIGMAR1 gene mutation and mitochondrial dysfunction in amyotrophic lateral sclerosis, J. Pharmacol. Sci., 127, 36, 10.1016/j.jphs.2014.12.012 · DOI
  38. Gonzalez-Perez, 2015, Identification of rare protein disulfide isomerase gene variants in amyotrophic lateral sclerosis patients, Gene, 566, 158, 10.1016/j.gene.2015.04.035 · DOI
  39. Grosskreutz, 2010, Calcium dysregulation in amyotrophic lateral sclerosis, Cell Calcium, 47, 165, 10.1016/j.ceca.2009.12.002 · DOI
  40. Gruszczynska-Biegala, 2013, Native STIM2 and ORAI1 proteins form a calcium-sensitive and thapsigargin-insensitive complex in cortical neurons, J. Neurochem., 126, 727, 10.1111/jnc.12320 · DOI
  41. Guardia-Laguarta, 2014, Alpha-Synuclein is localized to mitochondria-associated ER membranes, J. Neurosci., 34, 249, 10.1523/JNEUROSCI.2507-13.2014 · DOI · Paper page
  42. Halloran, 2013, The role of S-nitrosylation and S-glutathionylation of protein disulphide isomerase in protein misfolding and neurodegeneration, Int. J. Cell Biol., 2013, 797914, 10.1155/2013/797914 · DOI
  43. Harraz, 2008, SOD1 mutations disrupt redox-sensitive Rac regulation of NADPH oxidase in a familial ALS model, J. Clin. Invest., 118, 659
  44. Haun, 2013, S-nitrosylation of dynamin-related protein 1 mediates mutant huntingtin-induced mitochondrial fragmentation and neuronal injury in Huntington's disease, Antioxid. Redox Signal., 19, 1173, 10.1089/ars.2012.4928 · DOI
  45. Hawkins, 2010, S-glutathionylation activates STIM1 and alters mitochondrial homeostasis, J. Cell Biol., 190, 391, 10.1083/jcb.201004152 · DOI
  46. Hayashi, 2007, Sigma-1 receptor chaperones at the ER-mitochondrion interface regulate Ca(2+) signaling and cell survival, Cell, 131, 596, 10.1016/j.cell.2007.08.036 · DOI · Paper page
  47. Haynes, 2004, Degradation of misfolded proteins prevents ER-derived oxidative stress and cell death, Mol. Cell, 15, 767, 10.1016/j.molcel.2004.08.025 · DOI
  48. Hedskog, 2013, Modulation of the endoplasmic reticulum-mitochondria interface in Alzheimer's disease and related models, Proc. Natl. Acad. Sci. U. S. A., 110, 7916, 10.1073/pnas.1300677110 · DOI · Paper page
  49. Igoudjil, 2011, In vivo pathogenic role of mutant SOD1 localized in the mitochondrial intermembrane space, J. Neurosci., 31, 15826, 10.1523/JNEUROSCI.1965-11.2011 · DOI
  50. Israelson, 2010, Misfolded mutant SOD1 directly inhibits VDAC1 conductance in a mouse model of inherited ALS, Neuron, 67, 575, 10.1016/j.neuron.2010.07.019 · DOI
  51. Jahn, 2006, Temporospatial coupling of networked synaptic activation of AMPA-type glutamate receptor channels and calcium transients in cultured motoneurons, Neuroscience, 142, 1019, 10.1016/j.neuroscience.2006.07.034 · DOI
  52. Janiak, 1994, Assembly of Bcl-2 into microsomal and outer mitochondrial membranes, J. Biol. Chem., 269, 9842, 10.1016/S0021-9258(17)36960-0 · DOI
  53. Janiszewski, 2005, Regulation of NAD(P)H oxidase by associated protein disulfide isomerase in vascular smooth muscle cells, J. Biol. Chem., 280, 40813, 10.1074/jbc.M509255200 · DOI
  54. Jaronen, 2014, ER stress and unfolded protein response in amyotrophic lateral sclerosis-a controversial role of protein disulphide isomerase, Front. Cell. Neurosci., 8, 402, 10.3389/fncel.2014.00402 · DOI
  55. Jeon, 2014, Potential effect of S-nitrosylated protein disulfide isomerase on mutant SOD1 aggregation and neuronal cell death in amyotrophic lateral sclerosis, Mol. Neurobiol., 49, 796, 10.1007/s12035-013-8562-z · DOI
  56. Johnson, 2010, Exome sequencing reveals VCP mutations as a cause of familial ALS, Neuron, 68, 857, 10.1016/j.neuron.2010.11.036 · DOI · Paper page
  57. Johnson, 2014, Mutations in the CHCHD10 gene are a common cause of familial amyotrophic lateral sclerosis, Brain, 137, 10.1093/brain/awu265 · DOI
  58. Johnson, 2014, Mutations in the Matrin 3 gene cause familial amyotrophic lateral sclerosis, Nat. Neurosci., 17, 664, 10.1038/nn.3688 · DOI
  59. Kakizawa, 2012, Nitric oxide-induced calcium release via ryanodine receptors regulates neuronal function, EMBO J., 31, 417, 10.1038/emboj.2011.386 · DOI
  60. Kanekura, 2009, ER stress and unfolded protein response in amyotrophic lateral sclerosis, Mol. Neurobiol., 39, 81, 10.1007/s12035-009-8054-3 · DOI
  61. Kawamata, 2008, Different regulation of wild-type and mutant Cu, Zn superoxide dismutase localization in mammalian mitochondria, Hum. Mol. Genet., 17, 3303, 10.1093/hmg/ddn226 · DOI
  62. Kawamata, 2014, Abnormal intracellular calcium signaling and SNARE-dependent exocytosis contributes to SOD1G93A astrocyte-mediated toxicity in amyotrophic lateral sclerosis, J. Neurosci., 34, 2331, 10.1523/JNEUROSCI.2689-13.2014 · DOI · Paper page
  63. Kim, 2013, VCP is essential for mitochondrial quality control by PINK1/Parkin and this function is impaired by VCP mutations, Neuron, 78, 65, 10.1016/j.neuron.2013.02.029 · DOI
  64. Kiskinis, 2014, Pathways disrupted in human ALS motor neurons identified through genetic correction of mutant SOD1, Cell Stem Cell, 14, 781, 10.1016/j.stem.2014.03.004 · DOI · Paper page
  65. Kornmann, 2010, ERMES-mediated ER-mitochondria contacts: molecular hubs for the regulation of mitochondrial biology, J. Cell Sci., 123, 1389, 10.1242/jcs.058636 · DOI
  66. Kwok, 2013, Association studies indicate that protein disulfide isomerase is a risk factor in amyotrophic lateral sclerosis, Free Radic. Biol. Med., 58, 81, 10.1016/j.freeradbiomed.2013.01.001 · DOI
  67. Laurindo, 2008, Novel role of protein disulfide isomerase in the regulation of NADPH oxidase activity: pathophysiological implications in vascular diseases, Antioxid. Redox Signal., 10, 1101, 10.1089/ars.2007.2011 · DOI · Paper page
  68. Lautenschlager, 2013, Overexpression of human mutated G93A SOD1 changes dynamics of the ER mitochondria calcium cycle specifically in mouse embryonic motor neurons, Exp. Neurol., 247, 91, 10.1016/j.expneurol.2013.03.027 · DOI
  69. Magrane, 2009, Mutant SOD1 in neuronal mitochondria causes toxicity and mitochondrial dynamics abnormalities, Hum. Mol. Genet., 18, 4552, 10.1093/hmg/ddp421 · DOI
  70. Marangi, 2015, Genetic causes of amyotrophic lateral sclerosis: new genetic analysis methodologies entailing new opportunities and challenges, Brain Res., 1607, 75, 10.1016/j.brainres.2014.10.009 · DOI
  71. Marden, 2007, Redox modifier genes in amyotrophic lateral sclerosis in mice, J. Clin. Invest., 117, 2913, 10.1172/JCI31265 · DOI · Paper page
  72. Mattiazzi, 2002, Mutated human SOD1 causes dysfunction of oxidative phosphorylation in mitochondria of transgenic mice, J. Biol. Chem., 277, 29626, 10.1074/jbc.M203065200 · DOI
  73. Meng, 2011, Oxidation of the cysteine-rich regions of parkin perturbs its E3 ligase activity and contributes to protein aggregation, Mol. Neurodegener., 6, 34, 10.1186/1750-1326-6-34 · DOI
  74. Morotz, 2012, Amyotrophic lateral sclerosis-associated mutant VAPBP56S perturbs calcium homeostasis to disrupt axonal transport of mitochondria, Hum. Mol. Genet., 21, 1979, 10.1093/hmg/dds011 · DOI
  75. Moustaqim-Barrette, 2014, The amyotrophic lateral sclerosis 8 protein, VAP, is required for ER protein quality control, Hum. Mol. Genet., 23, 1975, 10.1093/hmg/ddt594 · DOI
  76. Nishimura, 2004, A mutation in the vesicle-trafficking protein VAPB causes late-onset spinal muscular atrophy and amyotrophic lateral sclerosis, Am. J. Hum. Genet., 75, 822, 10.1086/425287 · DOI · Paper page
  77. Nishitoh, 2008, ALS-linked mutant SOD1 induces ER stress- and ASK1-dependent motor neuron death by targeting Derlin-1, Genes Dev., 22, 1451, 10.1101/gad.1640108 · DOI
  78. Noguchi, 2005, ATPase activity of p97/valosin-containing protein is regulated by oxidative modification of the evolutionally conserved cysteine 522 residue in Walker A motif, J. Biol. Chem., 280, 41332, 10.1074/jbc.M509700200 · DOI
  79. Osman, 2014, Matrin 3 co-immunoprecipitates with the heat shock proteins glucose-regulated protein 78 (GRP78), GRP75 and glutathione S-transferase pi isoform 2 (GSTpi2) in thymoma cells, Biochimie, 101, 208, 10.1016/j.biochi.2014.01.015 · DOI
  80. Palomo, 2015, Exploring new pathways of neurodegeneration in ALS: the role of mitochondria quality control, Brain Res., 1607, 36, 10.1016/j.brainres.2014.09.065 · DOI
  81. Parone, 2013, Enhancing mitochondrial calcium buffering capacity reduces aggregation of misfolded SOD1 and motor neuron cell death without extending survival in mouse models of inherited amyotrophic lateral sclerosis, J. Neurosci., 33, 4657, 10.1523/JNEUROSCI.1119-12.2013 · DOI
  82. Pasinelli, 2004, Amyotrophic lateral sclerosis-associated SOD1 mutant proteins bind and aggregate with Bcl-2 in spinal cord mitochondria, Neuron, 43, 19, 10.1016/j.neuron.2004.06.021 · DOI
  83. Pedrini, 2010, ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2, Hum. Mol. Genet., 19, 2974, 10.1093/hmg/ddq202 · DOI
  84. Peretti, 2008, Coordinated lipid transfer between the endoplasmic reticulum and the Golgi complex requires the VAP proteins and is essential for Golgi-mediated transport, Mol. Biol. Cell, 19, 3871, 10.1091/mbc.E08-05-0498 · DOI
  85. Prause, 2013, Altered localization, abnormal modification and loss of function of Sigma receptor-1 in amyotrophic lateral sclerosis, Hum. Mol. Genet., 22, 1581, 10.1093/hmg/ddt008 · DOI
  86. Prell, 2012, The unfolded protein response in models of human mutant G93A amyotrophic lateral sclerosis, Eur. J. Neurosci., 35, 652, 10.1111/j.1460-9568.2012.08008.x · DOI
  87. Ranieri, 2013, Mitochondrial fusion proteins and human diseases, Neurol. Res. Int., 2013, 293893, 10.1155/2013/293893 · DOI
  88. Rasola, 2011, Mitochondrial permeability transition in Ca(2+)-dependent apoptosis and necrosis, Cell Calcium, 50, 222, 10.1016/j.ceca.2011.04.007 · DOI
  89. Rizzuto, 1993, Microdomains with high Ca2+ close to IP3-sensitive channels that are sensed by neighboring mitochondria, Science, 262, 744, 10.1126/science.8235595 · DOI
  90. Rizzuto, 2004, Flirting in little space: the ER/mitochondria Ca2+ liaison, Sci. STKE, 2004, re1, 10.1126/stke.2152004re1 · DOI
  91. Rosen, 1993, Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis, Nature, 362, 59, 10.1038/362059a0 · DOI · Paper page
  92. Santos, 2009, Protein disulfide isomerase (PDI) associates with NADPH oxidase and is required for phagocytosis of Leishmania chagasi promastigotes by macrophages, J. Leukoc. Biol., 86, 989, 10.1189/jlb.0608354 · DOI
  93. Sasaki, 2010, Endoplasmic reticulum stress in motor neurons of the spinal cord in sporadic amyotrophic lateral sclerosis, J. Neuropathol. Exp. Neurol., 69, 346, 10.1097/NEN.0b013e3181d44992 · DOI · Paper page
  94. Saxena, 2009, A role for motoneuron subtype-selective ER stress in disease manifestations of FALS mice, Nat. Neurosci., 12, 627, 10.1038/nn.2297 · DOI · Paper page
  95. Son, 2007, Overexpression of CCS in G93A-SOD1 mice leads to accelerated neurological deficits with severe mitochondrial pathology, Proc. Natl. Acad. Sci. U. S. A., 104, 6072, 10.1073/pnas.0610923104 · DOI
  96. Son, 2008, Isolated cytochrome c oxidase deficiency in G93A SOD1 mice over-expressing CCS protein, J. Biol. Chem., 283, 12267, 10.1074/jbc.M708523200 · DOI
  97. Staats, 2012, Dantrolene is neuroprotective in vitro, but does not affect survival in SOD1(G(9)(3)A) mice, Neuroscience, 220, 26, 10.1016/j.neuroscience.2012.06.050 · DOI
  98. Stoica, 2014, ER-mitochondria associations are regulated by the VAPB-PTPIP51 interaction and are disrupted by ALS/FTD-associated TDP-43, Nat. Commun., 5, 3996, 10.1038/ncomms4996 · DOI
  99. Sun, 2013, Oxygen-coupled redox regulation of the skeletal muscle ryanodine receptor/Ca2+ release channel (RyR1): sites and nature of oxidative modification, J. Biol. Chem., 288, 22961, 10.1074/jbc.M113.480228 · DOI
  100. Sundaramoorthy, 2013, Extracellular wildtype and mutant SOD1 induces ER-Golgi pathology characteristic of amyotrophic lateral sclerosis in neuronal cells, Cell. Mol. Life Sci., 70, 4181, 10.1007/s00018-013-1385-2 · DOI
  101. Tadic, 2014, The ER mitochondria calcium cycle and ER stress response as therapeutic targets in amyotrophic lateral sclerosis, Front. Cell. Neurosci., 8, 147, 10.3389/fncel.2014.00147 · DOI
  102. Tan, 2014, Role of mitochondria in mutant SOD1 linked amyotrophic lateral sclerosis, Biochim. Biophys. Acta, 1842, 1295, 10.1016/j.bbadis.2014.02.009 · DOI
  103. Teuling, 2007, Motor neuron disease-associated mutant vesicle-associated membrane protein-associated protein (VAP) B recruits wild-type VAPs into endoplasmic reticulum-derived tubular aggregates, J. Neurosci., 27, 9801, 10.1523/JNEUROSCI.2661-07.2007 · DOI · Paper page
  104. Urushitani, 2008, The endoplasmic reticulum-Golgi pathway is a target for translocation and aggregation of mutant superoxide dismutase linked to ALS, FASEB J., 22, 2476, 10.1096/fj.07-092783 · DOI · Paper page
  105. van Es, 2008, Genetic variation in DPP6 is associated with susceptibility to amyotrophic lateral sclerosis, Nat. Genet., 40, 29, 10.1038/ng.2007.52 · DOI
  106. van Vliet, 2014, New functions of mitochondria associated membranes in cellular signaling, Biochim. Biophys. Acta, 1843, 2253, 10.1016/j.bbamcr.2014.03.009 · DOI · Paper page
  107. Vance, 2014, MAM (mitochondria-associated membranes) in mammalian cells: lipids and beyond, Biochim. Biophys. Acta, 1841, 595, 10.1016/j.bbalip.2013.11.014 · DOI · Paper page
  108. Vijayvergiya, 2005, Mutant superoxide dismutase 1 forms aggregates in the brain mitochondrial matrix of amyotrophic lateral sclerosis mice, J. Neurosci., 25, 2463, 10.1523/JNEUROSCI.4385-04.2005 · DOI
  109. Vollrath, 2014, Loss of function of the ALS protein SigR1 leads to ER pathology associated with defective autophagy and lipid raft disturbances, Cell Death Dis., 5, 10.1038/cddis.2014.243 · DOI
  110. Walker, 2011, Mechanisms of neuroprotection by protein disulphide isomerase in amyotrophic lateral sclerosis, Neurol. Res. Int., 2011, 317340, 10.1155/2011/317340 · DOI
  111. Walker, 2010, Protein disulphide isomerase protects against protein aggregation and is S-nitrosylated in amyotrophic lateral sclerosis, Brain, 133, 105, 10.1093/brain/awp267 · DOI
  112. Walker, 2013, ALS-associated TDP-43 induces endoplasmic reticulum stress, which drives cytoplasmic TDP-43 accumulation and stress granule formation, PLoS One, 8, 10.1371/journal.pone.0081170 · DOI
  113. Wang, 2011, The unfolded protein response in familial amyotrophic lateral sclerosis, Hum. Mol. Genet., 20, 1008, 10.1093/hmg/ddq546 · DOI
  114. Waterham, 2007, A lethal defect of mitochondrial and peroxisomal fission, N. Engl. J. Med., 356, 1736, 10.1056/NEJMoa064436 · DOI · Paper page
  115. Yao, 2004, Nitrosative stress linked to sporadic Parkinson's disease: S-nitrosylation of parkin regulates its E3 ubiquitin ligase activity, Proc. Natl. Acad. Sci. U. S. A., 101, 10810, 10.1073/pnas.0404161101 · DOI
  116. Zhang, 2014, Aggregation-prone c9FTD/ALS poly(GA) RAN-translated proteins cause neurotoxicity by inducing ER stress, Acta Neuropathol., 128, 505, 10.1007/s00401-014-1336-5 · DOI

Cited by

Sorted by citations

See all 76

Metadata

Authors
Manfredi, G., & Kawamata, H.
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2016-06
Volume
90
Pages
35-42
ISSN
0969-9961
DOI
10.1016/j.nbd.2015.08.004
PMC
PMC4754163
Cited by
76
References
8
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Funders
  • NIH/NINDS (2R01NS051419-05, 1R01NS062055-01, 1R01NS084486-01)
  • MDA (255345)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review