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Arc/Arg3.1 regulates an endosomal pathway essential for activity-dependent β-amyloid generation.

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Arc/Arg3.1 regulates an endosomal pathway essential for activity-dependent β-amyloid generation. / Wu, Jing; Petralia, Ronald S; Kurushima, Hideaki; Patel, Hiral; Jung, Mi-young; Volk, Lenora; Chowdhury, Shoaib; Shepherd, Jason D; Dehoff, Marlin; Li, Yueming; Kuhl, Dietmar; Huganir, Richard L; Price, Donald L; Scannevin, Robert; Troncoso, Juan C; Wong, Philip C; Worley, Paul F.

in: CELL, Jahrgang 147, Nr. 3, 3, 2011, S. 615-628.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Wu, J, Petralia, RS, Kurushima, H, Patel, H, Jung, M, Volk, L, Chowdhury, S, Shepherd, JD, Dehoff, M, Li, Y, Kuhl, D, Huganir, RL, Price, DL, Scannevin, R, Troncoso, JC, Wong, PC & Worley, PF 2011, 'Arc/Arg3.1 regulates an endosomal pathway essential for activity-dependent β-amyloid generation.', CELL, Jg. 147, Nr. 3, 3, S. 615-628. <http://www.ncbi.nlm.nih.gov/pubmed/22036569?dopt=Citation>

APA

Wu, J., Petralia, R. S., Kurushima, H., Patel, H., Jung, M., Volk, L., Chowdhury, S., Shepherd, J. D., Dehoff, M., Li, Y., Kuhl, D., Huganir, R. L., Price, D. L., Scannevin, R., Troncoso, J. C., Wong, P. C., & Worley, P. F. (2011). Arc/Arg3.1 regulates an endosomal pathway essential for activity-dependent β-amyloid generation. CELL, 147(3), 615-628. [3]. http://www.ncbi.nlm.nih.gov/pubmed/22036569?dopt=Citation

Vancouver

Wu J, Petralia RS, Kurushima H, Patel H, Jung M, Volk L et al. Arc/Arg3.1 regulates an endosomal pathway essential for activity-dependent β-amyloid generation. CELL. 2011;147(3):615-628. 3.

Bibtex

@article{6e0b630cbd9a4b64a344edcb66c0a93c,
title = "Arc/Arg3.1 regulates an endosomal pathway essential for activity-dependent β-amyloid generation.",
abstract = "Assemblies of ?-amyloid (A?) peptides are pathological mediators of Alzheimer's Disease (AD) and are produced by the sequential cleavages of amyloid precursor protein (APP) by ?-secretase (BACE1) and ?-secretase. The generation of A? is coupled to neuronal activity, but the molecular basis is unknown. Here, we report that the immediate early gene Arc is required for activity-dependent generation of A?. Arc is a postsynaptic protein that recruits endophilin2/3 and dynamin to early/recycling endosomes that traffic AMPA receptors to reduce synaptic strength in both hebbian and non-hebbian forms of plasticity. The Arc-endosome also traffics APP and BACE1, and Arc physically associates with presenilin1 (PS1) to regulate ?-secretase trafficking and confer activity dependence. Genetic deletion of Arc reduces A? load in a transgenic mouse model of AD. In concert with the finding that patients with AD can express anomalously high levels of Arc, we hypothesize that Arc participates in the pathogenesis of AD.",
keywords = "Animals, Humans, Mice, Mice, Knockout, Nerve Tissue Proteins/*metabolism, Endosomes/*metabolism, Alzheimer Disease/*metabolism, Amyloid beta-Protein Precursor/*metabolism, Cell Membrane/metabolism, Cytoskeletal Proteins/*metabolism, *Protein Transport, Animals, Humans, Mice, Mice, Knockout, Nerve Tissue Proteins/*metabolism, Endosomes/*metabolism, Alzheimer Disease/*metabolism, Amyloid beta-Protein Precursor/*metabolism, Cell Membrane/metabolism, Cytoskeletal Proteins/*metabolism, *Protein Transport",
author = "Jing Wu and Petralia, {Ronald S} and Hideaki Kurushima and Hiral Patel and Mi-young Jung and Lenora Volk and Shoaib Chowdhury and Shepherd, {Jason D} and Marlin Dehoff and Yueming Li and Dietmar Kuhl and Huganir, {Richard L} and Price, {Donald L} and Robert Scannevin and Troncoso, {Juan C} and Wong, {Philip C} and Worley, {Paul F}",
year = "2011",
language = "English",
volume = "147",
pages = "615--628",
journal = "CELL",
issn = "0092-8674",
publisher = "Cell Press",
number = "3",

}

RIS

TY - JOUR

T1 - Arc/Arg3.1 regulates an endosomal pathway essential for activity-dependent β-amyloid generation.

AU - Wu, Jing

AU - Petralia, Ronald S

AU - Kurushima, Hideaki

AU - Patel, Hiral

AU - Jung, Mi-young

AU - Volk, Lenora

AU - Chowdhury, Shoaib

AU - Shepherd, Jason D

AU - Dehoff, Marlin

AU - Li, Yueming

AU - Kuhl, Dietmar

AU - Huganir, Richard L

AU - Price, Donald L

AU - Scannevin, Robert

AU - Troncoso, Juan C

AU - Wong, Philip C

AU - Worley, Paul F

PY - 2011

Y1 - 2011

N2 - Assemblies of ?-amyloid (A?) peptides are pathological mediators of Alzheimer's Disease (AD) and are produced by the sequential cleavages of amyloid precursor protein (APP) by ?-secretase (BACE1) and ?-secretase. The generation of A? is coupled to neuronal activity, but the molecular basis is unknown. Here, we report that the immediate early gene Arc is required for activity-dependent generation of A?. Arc is a postsynaptic protein that recruits endophilin2/3 and dynamin to early/recycling endosomes that traffic AMPA receptors to reduce synaptic strength in both hebbian and non-hebbian forms of plasticity. The Arc-endosome also traffics APP and BACE1, and Arc physically associates with presenilin1 (PS1) to regulate ?-secretase trafficking and confer activity dependence. Genetic deletion of Arc reduces A? load in a transgenic mouse model of AD. In concert with the finding that patients with AD can express anomalously high levels of Arc, we hypothesize that Arc participates in the pathogenesis of AD.

AB - Assemblies of ?-amyloid (A?) peptides are pathological mediators of Alzheimer's Disease (AD) and are produced by the sequential cleavages of amyloid precursor protein (APP) by ?-secretase (BACE1) and ?-secretase. The generation of A? is coupled to neuronal activity, but the molecular basis is unknown. Here, we report that the immediate early gene Arc is required for activity-dependent generation of A?. Arc is a postsynaptic protein that recruits endophilin2/3 and dynamin to early/recycling endosomes that traffic AMPA receptors to reduce synaptic strength in both hebbian and non-hebbian forms of plasticity. The Arc-endosome also traffics APP and BACE1, and Arc physically associates with presenilin1 (PS1) to regulate ?-secretase trafficking and confer activity dependence. Genetic deletion of Arc reduces A? load in a transgenic mouse model of AD. In concert with the finding that patients with AD can express anomalously high levels of Arc, we hypothesize that Arc participates in the pathogenesis of AD.

KW - Animals

KW - Humans

KW - Mice

KW - Mice, Knockout

KW - Nerve Tissue Proteins/metabolism

KW - Endosomes/metabolism

KW - Alzheimer Disease/metabolism

KW - Amyloid beta-Protein Precursor/metabolism

KW - Cell Membrane/metabolism

KW - Cytoskeletal Proteins/metabolism

KW - Protein Transport

KW - Animals

KW - Humans

KW - Mice

KW - Mice, Knockout

KW - Nerve Tissue Proteins/metabolism

KW - Endosomes/metabolism

KW - Alzheimer Disease/metabolism

KW - Amyloid beta-Protein Precursor/metabolism

KW - Cell Membrane/metabolism

KW - Cytoskeletal Proteins/metabolism

KW - Protein Transport

M3 - SCORING: Journal article

VL - 147

SP - 615

EP - 628

JO - CELL

JF - CELL

SN - 0092-8674

IS - 3

M1 - 3

ER -