The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
Effects of PS1 Deficiency on Membrane Protein Trafficking in Neurons
Open accessAbstract
We have examined the trafficking and metabolism of the beta-amyloid precursor protein (APP), an APP homolog (APLP1), and TrkB in neurons that lack PS1. We report that PS1-deficient neurons fail to secrete Abeta, and that the rate of appearance of soluble APP derivatives in the conditioned medium is increased. Remarkably, carboxyl-terminal fragments (CTFs) derived from APP and APLP1 accumulate in PS1-deficient neurons. Hence, PS1 plays a role in promoting intramembrane cleavage and/or degradation of membrane-bound CTFs. Moreover, the maturation of TrkB and BDNF-inducible TrkB autophosphorylation is severely compromised in neurons lacking PS1. We conclude that PS1 plays an essential role in modulating trafficking and metabolism of a selected set of membrane and secretory proteins in neurons.
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“Tail biopsy samples were used to isolate DNA to confirm the genotype of the strain using previously established primers by PCR93–95.”
From Serum amyloid P secreted by bone marrow adipocytes drives skeletal amyloidosis (2025) · cites this paper as [95]
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Citations
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“In addition, presenilins directly or indirectly regulate the trafficking and metabolism of select membrane proteins in neurons [86], as well as having a role in Mutation Phenotype Age of Onset References”
BackgroundPresenilin 1 deficiency impairs Aβ42-to-Aβ40- and angiotensin-converting activities of ACE
Gao, Y., Sun, Y., Islam, S., Nakamura, T., Tomita, T., Zou, K., & Michikawa, M. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1098034 · Cited by 4
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“Photoaffinity labeling experiments using C99-based substrates, each of which contained a single photocrosslinkable amino acid at residue positions 1 to 68, provided insights into how substrates bind to the enzyme (110).”
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Self-citationThe Value of Transgenic Models for the Study of Neurodegenerative Diseases
Price, D. L., Wong, P. C., Markowska, A. L., Thinakaran, G., Lee, M. K., Martin, L. J., Rothstein, J. D., Sisodia, S. S., & Borchelt, D. (2001) · Research and perspectives in Alzheimer's disease · doi:10.1007/978-3-662-04399-8_5 · Cited by 1
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Holback, S. (2009) · KTH Publication Database DiVA (KTH Royal Institute of Technology) · Cited by 1
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“Similar data were obtained for APP trafficking in the early compartments, sug gesting that the TLN accumulations (this study) and probably also the strong decrease of A~ secretion in PSI neurons (De Strooper et al. 1998; Naruse et al. 1998 ) are not due to aberrant trafficking in the early secretory pathway.”
BackgroundResultInfluentialThinakaran, G., Saura, C. A., Tomita, T., Honda, T., & Iwatsubo, T. (2001) · Birkhäuser Basel eBooks · doi:10.1007/978-3-0348-8225-5_19
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Adwan, L. I. (2013) · Digital Commons - URI (University of Rhode Island) · doi:10.23860/diss-adwan-lina-2013
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Genetics of early-onset Alzheimer disease
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Self-citationAdlerz, L. (2007) · KTH Publication Database DiVA (KTH Royal Institute of Technology)
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Selivanova, A. V. (2007) · Figshare
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“In addition, although experimental evidence concerning the roles of PS1 and APP in protein trafficking, such as TrkB (Naruse et al. 1998), telencephalin (Annaert et al.”
BackgroundChromosome Missegregation in Alzheimer's Disease Caused by Presenilin 1
Boeras, D. I. (2005) · Digital Commons - University of South Florida (University of South Florida)
Processing of the APP family by the α-secretases ADAM10 and TACE
Jacobsen, K. T. (2010) · KTH Publication Database DiVA (KTH Royal Institute of Technology)
A study of the role of presenilin (1) in regulating synaptic function at hippocampal synapses
Yu, L. M. Y. (2010) · UCL Discovery (University College London)
Gandy, S., Silva, O. A. B. D. C. E., Silva, E. D. C. E., Suzuki, T., Ehrlich, M. E., & Small, S. A. (2009) · Research and perspectives in Alzheimer's disease · doi:10.1007/978-3-540-87941-1_1
“In cells from PS1-deficient mice, delivery of multiple type-I proteins to the cell surface was observed to be disturbed; APP and the p75 neurotrophin receptor were among those missorted proteins ( Naruse et al. 1998 ).”
BackgroundMethod
Metadata
- Authors
- Naruse, S., Thinakaran, G., Luo, J.-J., Kusiak, J. W., Tomita, T., Iwatsubo, T., Qian, X., Ginty, D. D., Price, D. L., Borchelt, D. R., Wong, P. C., & Sisodia, S. S.
- Affiliations
- University of Chicago (US)
- Johns Hopkins University (US)
- National Institute on Aging (US)
- The University of Tokyo (JP)
- Corresponding author
- Sisodia, Sangram S
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 1998-11
- Volume
- 21
- Issue
- 5
- Pages
- 1213-1221
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W1994453752
- Cited by
- 355
- References
- 43
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 2 · 2023: 3 · 2022: 1 · 2021: 2 · 2020: 3 · 2019: 2 · 2018: 2 · 2017: 4 · 2016: 5 · 2015: 4 · 2014: 4 · 2013: 12 · 2012: 7
- FWCI
- 22.15
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Neuron (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (1PO1 AG 14248, P50AG005146, P01AG014248, AG 05146)
- National Institute of Neurological Disorders and Stroke (NS-20471)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- presenilin 1, APP, APLP1, amyloid-beta, carboxyl-terminal fragment, membrane protein trafficking, TrkB, brain-derived neurotrophic factor, autophosphorylation, intramembrane cleavage, protein degradation, Alzheimer's disease, neurons
- MeSH terms
- Alzheimer Disease, Animals, Cells, Cultured, Cerebral Cortex, Fetus, Membrane Proteins, Molecular Sequence Data, Neurons, Amyloid beta-Protein Precursor, Mice, Knockout, Mice, Presenilin-1
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