Neuronal sorting protein-related receptor sorLA/LR11 regulates processing of the amyloid precursor protein.

By O. Andersen, Juliane Reiche, Vanessa Schmidt, M. Gotthardt, Robert Spoelgen, J. Behlke, C. V. von Arnim, T. Breiderhoff, Pernille Jansen, Xin Wu and 9 more. Proceedings of the National Academy of Sciences of the United States of America, 2005

657 citations recorded by the source corpus.

Subfields: Cell Biology, Cellular and Molecular Neuroscience, Physiology

View Paper: https://www.semanticscholar.org/paper/17f8d1928821f8005b59b361ded9a9a051a53f5f

How researchers see this paper

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In Cell Biology

1. G. Bu
2. Philip C. Wong
3. D. Holtzman

In Cellular and Molecular Neuroscience

1. D. Holtzman
2. J. Herz
3. Dennis W. Dickson
4. G. Bu
5. Christian Haass
6. Sangram S. Sisodia
7. J. Long

In Physiology

1. D. Holtzman
2. G. Bu
3. J. Herz
4. Rudolph E. Tanzi
5. Philip C. Wong
6. Richard P. Mayeux
7. Richard O'Brien
8. Dennis W. Dickson

Citations in the corpus

• The genetics of Alzheimer disease. (2012, background): “These include, for example, SORL1 (sortilin-related receptor), which is a sorting receptor that regulates the intracellular trafficking of a variety of proteins, including APP (Andersen et al. 2005; Rogaeva et al. 2007).”
• Amyloid Precursor Protein Processing and Alzheimer’s Disease (2011, background): “SorLA, a member of the low density lipoprotein receptor superfamily, is one such adaptor protein and binds APP (Andersen et al. 2005) via its N-terminal complement-like domain and binds to the retromer complex via its vacuolar protein-sorting domain ( Jacobsen et al. 2001).”
• Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020, background): “Overexpression of SORLA in neuronal cells can block amyloidogenic processing and reduce Aβ production [485], whereas loss of SORLA increased extracellular Aβ levels and plaque deposition in several AD mouse models [486, 487].”
• The neuronal sortilin-related receptor SORL1 is genetically associated with Alzheimer disease (2007, background): “13 )) is reduced in brain tissue from individuals with Alzheimer disease and (ii) reductions in the expression of some of these proteins are associated with increased Aβ productio”
• The Role of Apolipoprotein E in Alzheimer’s Disease (2009, neutral): “LR11/ SorLA sequesters APP in the trans-Golgi network, decreasing the amount of APP in postGolgi compartments and the plasma membrane (Andersen et al., 2005; Schmidt et al., 2007).”
• Apolipoprotein E and its receptors in Alzheimer's disease: pathways, pathogenesis and therapy (2009, background): “and overexpression of SORLA in neurons shifts APP distribution to the Golgi compartment and decreases its processing to A&beta”
• Apolipoprotein E and apolipoprotein E receptors: normal biology and roles in Alzheimer disease. (2012, positive): “Importantly, a deletion of the Sorla gene in mice increases concentration of Ab in the brain (Andersen et al. 2005).”
• Trafficking and proteolytic processing of APP. (2012, background): “…et al. 2006). sorLA/LR11 is also genetically associatedwith AD and its steady-state levels are markedly reduced in the brains of patients with AD, further implicating this sortingmolecule in the physiological regulation of APPmetabolism (Andersen et al. 2005; Offe et al. 2006; Rogaeva et al. 2007).”