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Cited by 183

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

C‐terminal fragments of amyloid precursor protein exert neurotoxicity by inducing glycogen synthase kinase‐3β expression

Kim, Hye-Sun, Kim, Eun-Mee, Lee, Jean-Pyo, Park, Cheol Hyoung, Kim, Seonghan, Seo, Ji-Heui, Chang, Keun-A, Yu, Eunah, Jeong, Sung-Jin, Chong, Young Hae, Suh, Yoo-Hun·2003·The FASEB Journal
DOI 10.1096/fj.03-0106fje
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Abstract

The AICD (amyloid precursor protein [APP] intracellular domain) and C31, the caspase‐cleaved C‐terminal fragment of APP, have been found in the brains of patients with Alzheimer's disease (AD). Here, we demonstrate for the first time that the C‐terminal fragments of APP (AICD [C57, C59] and C31) exert neurotoxicity on differentiated PC 12 cells and rat primary cortical neurons by inducing the expression of glycogen synthase kinase 3β, forming a ternary complex with Fe65 and CP2/LSF/LBP1 in the nucleus, whereas deletion mutants and a point mutant with Y682G of the YENPTY domain, a Fe65 binding domain, do not. Moreover, expression of APP770 and Swedish mutant form of APP increased the levels of C‐terminal fragments of APP (APP‐CTs) in neuronal cells and also induced the up‐regulation of glycogen synthase kinase‐3β at both the mRNA and the protein levels. In addition, we show that CP2/LSF/LBP1 binding site (nt +0 to ∼+10) in human glycogen synthase kinase 3β promoter region is essential for the induction of the gene transcription by APP‐CTs. The neurotoxicities induced by APP‐CTs (AICD and C31) were accompanied by an increase in the active form of glycogen synthase knase‐3β, and by the induction of tau phosphorylation and a reduction in nuclear β‐catenin levels, and led to apoptosis.

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Crossref · 10.1096/fj.03-0106fje

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3 of 3 references verified0 citation errors · 0 not checkable

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  • AICD is a signaling molecule that can translocate to the nucleus and regulate expression of manifold genes, some involved in AD pathogenic mechanisms, cytoskeleton dynamics, cell cycle control, or synaptic plasticity.

    “AICD has gained consensus as signaling molecule that can translocate to the nucleus and regulate the expression of manifold genes, some of them involved in AD pathogenic mechanisms (Kim et al., 2003; Chang et al., 2006), but also in cytoskeleton dynamics, cell cycle control or synaptic plasticity.”

    From Emerging Alternative Proteinases in APP Metabolism and Alzheimer’s Disease Pathogenesis: A Focus on MT1-MMP and MT5-MMP (2019) · cites this paper as Kim et al., 2003

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Metadata

Authors
Kim, H.-S., Kim, E.-M., Lee, J.-P., Park, C. H., Kim, S., Seo, J.-H., Chang, K.-A., Yu, E., Jeong, S.-J., Chong, Y. H., & Suh, Y.-H.
Affiliations
  • Department of Pharmacology College of Medicine National Creative Research Initiative Center for Alzheimer's Dementia Neuroscience Research Institute MRC Seoul National University Seoul 110-799 South Korea
  • Department of Cell Biology Harvard Medical School Boston MA 02115 USA
  • Department of Microbiology College of Medicine Division of Neuroscience Medical Research Center Ewha Womans University 911-1, Mok-6-dong, Yangcheonku Seoul 158-056 South Korea
Venue
The FASEB Journal
Publisher
Wiley
Published
2003-08-15
Volume
17
Issue
13
Pages
1-28
ISSN
  • 0892-6638
  • 1530-6860
DOI
10.1096/fj.03-0106fje
Cited by
183
References
3
Language
en
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)

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