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Cited by 36

The DOI matches its Crossref record, with a small difference in title or year; 6 of the 6 references it cites were found in a registry or an index.

RETRACTED ARTICLE: VPS35 regulates tau phosphorylation and neuropathology in tauopathy

Vagnozzi, Alana N., Li, Jian-Guo, Chiu, Jin, Razmpour, Roshanak, Warfield, Rebecca, Ramirez, Servio H., Praticò, Domenico·2021·Molecular Psychiatry
DOI 10.1038/s41380-019-0453-xPMC PMC6949432
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  • Most in vivo mouse studies of retromer in AD have been performed in transgenic mice overexpressing human mutations in APP and PSEN1/2 or FTD-associated mutations in the tau gene MAPT.

    “most in vivo mouse studies have been performed in transgenic mice engineered to overexpress human mutations in APP and PSEN1/2 (Wen et al., 2011; Li et al., 2019a) or FTD-associated mutations in the tau gene MAPT (Vagnozzi et al., 2019; Carosi et al., 2020).”

    From The neuronal retromer can regulate both neuronal and microglial phenotypes of Alzheimer's disease (2022) · cites this paper as Vagnozzi et al., 2019

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Research works printed but not linked: 35

  1. O’Brien RJ, Wong PC. Amyloid precursor protein processing and Alzheimer’s disease. Annu Rev Neurosci 2011;34:185–204. · DOI · Paper page
  2. Choy RW-Y, Chen Z, Schekman R. Amyloid precursor protein traffics from the cell surface via endosomes for amyloid beta production in the trans-Golgi network. Proc Natl Acad Sci USA. 2012;109:E2077–E2088. · DOI
  3. Trousdale C, Kim K. Retromer: structure, function, and roles in mammalian disease. Eur J Cell Biol 2015;94:513–21. · DOI
  4. Wang S, Bellen HJ. The retromer complex in development and disease. Development. 2015;142:2392–6. · DOI
  5. Temkin P, Lauffer B, Jager S, Cimermancic P, Krogan NJ, von Zastrow M. SNX27-mediates retromer tubule entry and endosome-to-plasma membrane trafficking of signaling receptors. Nat Cell Biol 2011;13:715–21. · DOI · Paper page
  6. Nielsen MS, Gustafsen C, Madsen P, Nyengaard JR, Hermey G, et al. Sorting by the cytoplasmic domain of the amyloid precursor protein binding receptor SorLA. Mol Cell Biol 2007;27:6842–51. · DOI · Paper page
  7. Fjorback AW, Seaman M, Gustafsen C, Mehmedbasic A, Gokool S, et al. Retromer binds the FANSHY soring motif in SorLA to regulate amyloid precursor protein sorting and processing. J Neurosci 2012;32:1467–80. · DOI · Paper page
  8. Small SA, Kent K, Pierce A, Leung C, Kang MS, et al. Model-guided microarray implicates the retromer complex in Alzheimer’s disease. Ann Neurol 2005;58:909–19. · DOI · Paper page
  9. Vardarajan BN, Bruesegem SY, Harbour ME, Inzelberg R, Friedland R, et al. Identification of Alzheimer’s disease-associated variants in genes that regulate retromer function. Neurobiol Aging. 2012;33:2231.e15–2231.e30. · DOI · Paper page
  10. Chu J, Praticò D. The retromer complex system in a transgenic mouse model of AD: influence of age. Neurobiol Aging 2017;52:32–38. · DOI
  11. Chu J, Giannopoulos PF, Ceballos-Diaz C, Golde TE, Pratico D. Adeno-associated virus-mediated brain delivery of 5-lipoxygenase modulates the AD-like phenotype of APP mice. Mol Neurodegener 2012;7:1. · DOI
  12. Vagnozzi AN, Giannopoulos PF, Praticò D. Brain 5-lipoxygenase overexpression worsens memory, synaptic integrity, and tau pathology in the P301S mice. Aging Cell 2018;17:e12695. · DOI
  13. Di Meco A, Lauretti E, Vagnozzi AN, Praticò D. Zileuton restores memory impairments and reverses amyloid and tau pathology in aged Alzheimer’s disease mice. Neurobiol Aging. 2014;35:2458–64. · DOI
  14. Li JG, Chu J, Barrero C, Merali S, Praticò D. Homocysteine exacerbates β‐amyloid pathology, tau pathology, and cognitive deficit in a mouse model of Alzheimer disease with plaques and tangles. Ann Neurol 2014;75:851–63. · DOI
  15. Vagnozzi AN, Giannopoulos PF, Praticò D. The direct role of 5-lipoxygenase on tau pathology, synaptic integrity and cognition in a mouse model of tauopathy. Transl Psychiatry 2017;18:1288. · DOI
  16. Lauretti E, Li JG, Di Meco A, Praticò D. Glucose deficit triggers tau pathology and synaptic dysfunction in a tauopathy mouse model. Transl Psychiatry 2017;7:e1020. · DOI
  17. Li, JG, Chu, J, Praticò, D. Downregulation of autophagy by 12/15Lipoxygenase worsens the phenotype of an Alzheimer’s disease mouse model with plaques, tangles, and memory impairments. Mol Psychiatry. 2018. https://doi.org/10.1038/s41380-018-0268-1. · DOI
  18. Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) Method. Methods 2001;25:402–8. · DOI · Paper page
  19. Giannopoulos, PF, Chu, J, Praticò, D. Learning impairments, memory deficits, and neuropathology in aged tau transgenic mice are dependent on leukotrienes biosynthesis: role of the cdk5 kinase pathway. Mol Neurobiol. 2018. https://doi.org/10.1007/s12035-018-1124-7. · DOI
  20. Miura E, Hasegawa T, Konno M, Suzuki M, Sugeno N, et al. VPS35 dysfunction impairs lysosomal degradation of α-synuclein and exacerbates neurotoxicity in a Drosophila model of Parkinson’s disease. Neurobiol Dis 2014;71:1–13. · DOI
  21. Chu J, Li JG, Hoffman NE, Stough AM, Madesh M, Praticò D. Regulation of gamma-secretase activating protein by the 5Lipoxygenase: in vitro and in vivo evidence. Sci Rep 2015;5:11086. · DOI
  22. Lauretti E, Praticò D. Glucose deprivation increases tau phosphorylation via P38 mitogen-activated protein kinase. Aging Cell. 2015;14:1067–74. · DOI
  23. Mecozzi VJ, Berman DE, Simoes S, Vetanovetz C, Awal MR, et al. Pharmacological chaperones stabilize retromer to limit APP processing. Nat Chem Biol 2014;10:443–9. · DOI · Paper page
  24. Kim E, Lee Y, Lee HJ, Kim JS, Song BS, et al. Implication of mouse VPS26b-VPS29-VPS35 retromer complex in sortilin trafficking. Biochem Biophys Res Commun 2010;403:167–71. · DOI
  25. Lee MJ, Lee JH, Rubinsztein DC. Tau degradation: the ubiquitin-proteasome system versus the autophagy-lysosome system. Progr Neurobiol 2013;105:49–59. · DOI · Paper page
  26. Zhang Y, Chen X, Zhao Y, Ponnusamy M, Liu Y. The role of ubiquitin proteasomal system and autophagy-lysosomal pathway in Alzheimer’s disease. Rev Neurosci 2017;28:861–8. · DOI
  27. Zang JY, Liu SJ, Li HL, Wang JZ. Microtubule-associated protein tau is a substrate of ATP/Mg (2+)-dependent proteasome protease system. J Neural Transm 2005;112:547–55. · DOI
  28. Hamano T, Gendron TF, Causevic E, Yen SH, Lin WL, et al. Autophagic-lysosomal perturbation enhances tau aggregation in transfectants with induced wild-type tau expression. Eur J Neurosci. 2018;27:119–1130.
  29. Schuur M, Ikram MA, van Swieten JC, Isaacs A, Vergeer-Drop JM, et al. Cathepsin D gene and the risk of Alzheimer’s disease: a population-based study and meta-analysis. Neurobiol Aging. 2011;32:1607–1614. · DOI
  30. Chai, YL, Chong, JR, Weng, J, Howlett, D, Halsey, A, et al. Lysosomal cathepsin D is upregulated in Alzheimer’s disease neocortex and may be a marker for neurofibrillary degeneration. Brain Pathol. 2018. https://doi.org/10.1111/bpa.12631. · DOI · Paper page
  31. Follett J, Norwood SJ, Hamilton NA, Mohan M, Kovtun O. The VPS35 D620N mutation linked to Parkinson’s disease disrupts the cargo sorting function of retromer. Traffic. 2014;15:230–44. · DOI
  32. Seaman MNJ. Cargo‐selective endosomal sorting for retrieval to the Golgi requires retromer. J Cell Biol. 2004;165:111–22. · DOI · Paper page
  33. Kenessey A, Nacharaju P, Ko L, Yen S. Degradation of Tau by lysosomal enzyme cathepsin D: implication for alzheimer neurofibrillary degeneration. J Neurochem 1997;69:2026–38. · DOI
  34. Williams ET, Chen X, Moore DJ. VPS35, the retromer complex, and Parkinson’s disease. J Parkinsons Dis. 2017;7:219–33. · DOI
  35. Li JG, Chiu J, Praticò D. Full recovery of the Alzheimer’s disease phenotype by gain of function of Vacuolar Protein Sorting 35. Mol. Psychiatry. 2019. https://doi.org/10.1038/s41380-019-0364-x. (Epub ahead of print) · DOI

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Metadata

Authors
Vagnozzi, A. N., Li, J.-G., Chiu, J., Razmpour, R., Warfield, R., Ramirez, S. H., & Praticò, D.
Venue
Molecular Psychiatry
Publisher
Springer Science and Business Media LLC
Published
2019-07-09
Volume
26
Issue
11
Pages
6992-7005
ISSN
  • 1359-4184
  • 1476-5578
DOI
10.1038/s41380-019-0453-x
PMC
PMC6949432
Cited by
36
References
6
Language
en
Status
Retracted
Update notices
retraction (2023-01-25)
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