The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Disturbed Activation of Endoplasmic Reticulum Stress Transducers by Familial Alzheimer's Disease-linked Presenilin-1 Mutations
Open accessAbstract
Recent studies have shown independently that presenilin-1 (PS1) null mutants and familial Alzheimer's disease (FAD)-linked mutants should both down-regulate signaling of the unfolded protein response (UPR). However, it is difficult to accept that both mutants possess the same effects on the UPR. Furthermore, contrary to these observations, neither loss of PS1 and PS2 function nor expression of FAD-linked PS1 mutants were reported to have a discernable impact on the UPR. Therefore, re-examination and detailed analyses are needed to clarify the relationship between PS1 function and UPR signaling. Here, we report that PS1/PS2 null and dominant negative PS1 mutants, which are mutated at aspartate residue 257 or 385, did not affect signaling of the UPR. In contrast, FAD-linked PS1 mutants were confirmed to disturb UPR signaling by inhibiting activation of both Ire1alpha and ATF6, both of which are endoplasmic reticulum (ER) stress transducers in the UPR. Furthermore, PS1 mutants also disturbed activation of PERK (PKR-like ER kinase), which plays a crucial role in inhibiting translation during ER stress. Taken together, these observations suggested that PS1 mutations could affect signaling pathways controlled by each of the respective ER-stress transducers, possibly through a gain-of-function.
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Cites
Goate, A., Chartier-Harlin, M.-C., Mullan, M., Brown, J., Crawford, F., Fidani, L., Giuffra, L., Haynes, A., Irving, N., James, L., et al. (1991) · Nature · doi:10.1038/349704a0 · Cited by 4,659
Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease
Sherrington, R., Rogaev, E. I., Liang, Y., Rogaeva, E. A., Levesque, G., Ikeda, M., Chi, H., Lin, C., Li, G., Holman, K., et al. (1995) · Nature · doi:10.1038/375754a0 · Cited by 4,051
Self-citationCandidate gene for the chromosome 1 familial Alzheimer’s disease locus
Levy-Lahad, E., Wasco, W., Poorkaj, P., Romano, D. M., Oshima, J., Pettingell, W. H., Yu, C.-E., Jondro, P. D., Schmidt, S. D., Wang, K., et al. (1995) · Science · doi:10.1126/science.7638622 · Cited by 2,577
Rogaev, E. I., Sherrington, R., Rogaeva, E. A., Levesque, G., Ikeda, M., Liang, Y., Chi, H., Lin, C., Holman, K., Tsuda, T., et al. (1995) · Nature · doi:10.1038/376775a0 · Cited by 2,052
Self-citationHarding, H. P., Zhang, Y., Bertolotti, A., Zeng, H., & Ron, D. (2000) · Molecular Cell · doi:10.1016/s1097-2765(00)80330-5 · Cited by 2,021
ER Stress Induces Cleavage of Membrane-Bound ATF6 by the Same Proteases that Process SREBPs
Ye, J., Rawson, R. B., Komuro, R., Chen, X., Davé, U. P., Prywes, R., Brown, M. S., & Goldstein, J. L. (2000) · Molecular Cell · doi:10.1016/s1097-2765(00)00133-7 · Cited by 1,871
Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein
De Strooper, B., Saftig, P., Craessaerts, K., Vanderstichele, H., Guhde, G., Annaert, W., Von Figura, K., & Van Leuven, F. (1998) · Nature · doi:10.1038/34910 · Cited by 1,818
Mullan, M., Crawford, F., Axelman, K., Houlden, H., Lilius, L., Winblad, B., & Lannfelt, L. (1992) · Nature Genetics · doi:10.1038/ng0892-345 · Cited by 1,513
Chartier-Harlin, M.-C., Crawford, F., Houlden, H., Warren, A., Hughes, D., Fidani, L., Goate, A., Rossor, M., Roques, P., Hardy, J., et al. (1991) · Nature · doi:10.1038/353844a0 · Cited by 1,214
Yoshida, H., Okada, T., Haze, K., Yanagi, H., Yura, T., Negishi, M., & Mori, K. (2000) · Molecular and Cellular Biology · doi:10.1128/mcb.20.18.6755-6767.2000 · Cited by 934
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Cited by
Yoshida, H. (2007) · The FEBS Journal · doi:10.1111/j.1742-4658.2007.05639.x · Cited by 1,086
The unfolded protein response: A stress signaling pathway critical for health and disease
Zhang, K., & Kaufman, R. J. (2006) · Neurology · doi:10.1212/01.wnl.0000192306.98198.ec · Cited by 579
Unfolded proteins and endoplasmic reticulum stress in neurodegenerative disorders
Doyle, K. M., Kennedy, D., Gorman, A. M., Gupta, S., Healy, S. J. M., & Samali, A. (2011) · Journal of Cellular and Molecular Medicine · doi:10.1111/j.1582-4934.2011.01374.x · Cited by 321
mTORC1 serves ER stress-triggered apoptosis via selective activation of the IRE1–JNK pathway
Kato, H., Nakajima, S., Saito, Y., Takahashi, S., Katoh, R., & Kitamura, M. (2012) · Cell Death & Differentiation · doi:10.1038/cdd.2011.98 · Cited by 272
ER stress and UPR in Alzheimer’s disease: mechanisms, pathogenesis, treatments
Ajoolabady, A., Lindholm, D., Ren, J., & Pratico, D. (2022) · Cell Death & Disease · doi:10.1038/s41419-022-05153-5 · Cited by 261
Metadata
- Authors
- Katayama, T., Imaizumi, K., Honda, A., Yoneda, T., Kudo, T., Takeda, M., Mori, K., Rozmahel, R., Fraser, P., George-Hyslop, P. S., & Tohyama, M.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2001-11
- Volume
- 276
- Issue
- 46
- Pages
- 43446-43454
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2145112854
- Cited by
- 181
- References
- 10
- FWCI
- 2.48
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- CoChat. (2026). Citation check: Disturbed Activation of Endoplasmic Reticulum Stress Transducers by Familial Alzheimer's Disease-linked Presenilin-1 Mutations. https://app.cochat.ai/papers/10.1074/jbc.m104096200
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- Katayama, T., Imaizumi, K., Honda, A., Yoneda, T., Kudo, T., Takeda, M., Mori, K., Rozmahel, R., Fraser, P., George-Hyslop, P. S., & Tohyama, M. (2001). Disturbed Activation of Endoplasmic Reticulum Stress Transducers by Familial Alzheimer's Disease-linked Presenilin-1 Mutations. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m104096200
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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