Cited by 355Alzheimer's disease research and treatmentsCellular transport and secretionNeuroscience and Neuropharmacology Research

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Effects of PS1 Deficiency on Membrane Protein Trafficking in Neurons

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Naruse, Satoshi, Thinakaran, Gopal, Luo, Jin-Jun, Kusiak, John W, Tomita, Taisuke, Iwatsubo, Takeshi, Qian, Xiaozhong, Ginty, David D, Price, Donald L, Borchelt, David R, Wong, Philip C, Sisodia, Sangram S·1998·Neuron

DOI 10.1016/s0896-6273(00)80637-6

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Abstract

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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The presenilin-1 ΔE9 mutation results in reduced γ-secretase activity, but not total loss of PS1 function, in isogenic human stem cells
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“Protein blot analyses using CT15, an antibody specific for the C terminus of APP, revealed the accumulation of full-length APP and APP-CTFs (Fig. 4 A )i nNCT/ cells, results that are reminiscent of those obtained in studies of PS1 or PS1PS2 null cells (De Strooper et al., 1998; Naruse et al., 1998; Herreman et al., 20…”
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Nicastrin Is Required for γ-Secretase Cleavage of the Drosophila Notch Receptor
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Presenilin 1 mediates the turnover of telencephalin in hippocampal neurons via an autophagic degradative pathway
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H UMAN N EURODEGENERATIVE D ISEASE M ODELING U SING D ROSOPHILA
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Conditional Inactivation of Presenilin 1 Prevents Amyloid Accumulation and Temporarily Rescues Contextual and Spatial Working Memory Impairments in Amyloid Precursor Protein Transgenic Mice
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“In addition, PS1 deficiency in neurons accelerated the secretion of α- and β-secretase cleaved APP ectodomain [ 93 ].”
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“A role in trafficking of membrane proteins has been proposed for PS. APP trafficking as well as TrkB maturation and autophosphorylation are impaired in PS1–/– neurons, suggesting that TrkB is not correctly trafficked through the secretory pathway (Naruse et al. 1998).”
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“They are initially cleaved in the extracellular domain, either by a- or b-secretase, followed by PS1-dependent cleavage in the plane of the membrane, liberating a cytosolic fragment (AICD or AICD-like frag- ments).”
BackgroundInfluential
Presenilin-1 deficiency leads to loss of Cajal–Retzius neurons and cortical dysplasia similar to human type 2 lissencephaly
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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: Naruse, Satoshi
Thinakaran, Gopal
Luo, Jin-Jun
Kusiak, John W
Tomita, Taisuke
Iwatsubo, Takeshi
Qian, Xiaozhong
Ginty, David D
Borchelt, David R
Wong, Philip C
Sisodia, Sangram S
Venue: Neuron
Publisher: Elsevier BV
Published: 1998-11
Volume: 21
Issue: 5
Pages: 1213-1221
ISSN: 0896-6273 (ISSN-L)
DOI: 10.1016/s0896-6273(00)80637-6
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: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
creativecommons.org/licenses/by-nc-nd/4.0/ (vor, 892 d)
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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Effects of PS1 Deficiency on Membrane Protein Trafficking in Neurons

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