The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Presenilin Proteins Undergo Heterogeneous Endoproteolysis between Thr291and Ala299and Occur as Stable N- and C-Terminal Fragments in Normal and Alzheimer Brain Tissue
Open accessAbstract
Humans inheriting missense mutations in the presenilin (PS)1 and -2 genes undergo progressive cerebral deposition of the amyloid beta-protein at an early age and develop a clinically and pathologically severe form of familial Alzheimer's disease (FAD). Because PS1 mutations cause the most aggressive known form of AD, it is important to elucidate the structure and function of this multitransmembrane protein in the brain. Using a panel of region-specific PS antibodies, we characterized the presenilin polypeptides in mammalian tissues, including brains of normal, AD, and PS1-linked FAD subjects, and in transfected and nontransfected cell lines. Very little full-length PS1 or -2 was detected in brain and untransfected cells; instead the protein occurred as a heterogeneous array of stable N- and C-terminal proteolytic fragments that differed subtly among cell types and mammalian tissues. Sequencing of the major C-terminal fragment from PS1-transfected human 293 cells showed that the principal endoproteolytic cleavage occurs at and near Met298 in the proximal portion of the large hydrophilic loop. Full-length PS1 in these cells is quickly turned over (T1/2 approximately 60 min), in part to the two major fragments. The sizes and amounts of the PS fragments were not significantly altered in four FAD brains with the Cys410Tyr PS1 missense mutation. Our results indicate that presenilins are rapidly processed to N- and C-terminal fragments in both neural and nonneural cells and that interference with this processing is not an obligatory feature of FAD-causing mutations.
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Self-citationCandidate gene for the chromosome 1 familial Alzheimer’s disease locus
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Self-citationAmyloid β-peptide is produced by cultured cells during normal metabolism
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Self-citationREVIEWThe Gene Defects Responsible for Familial Alzheimer's Disease
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Cited by
Alzheimer's Disease: Genes, Proteins, and Therapy
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Self-citationTranslating cell biology into therapeutic advances in Alzheimer's disease
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Self-citationSkeletal and CNS Defects in Presenilin-1-Deficient Mice
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Self-citationA Portrait of Alzheimer Secretases--New Features and Familiar Faces
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ALZHEIMER'S DISEASE: Genetic Studies and Transgenic Models
Price, D. L., Tanzi, R. E., Borchelt, D. R., & Sisodia, S. S. (1998) · Annual Review of Genetics · doi:10.1146/annurev.genet.32.1.461 · Cited by 406
Metadata
- Authors
- Podlisny, M. B., Citron, M., Amarante, P., Sherrington, R., Xia, W., Zhang, J., Diehl, T., Levesque, G., Fraser, P., Haass, C., Koo, E. H. M., Seubert, P., St. George-Hyslop, P., Teplow, D. B., & Selkoe, D. J.
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 1997-01
- Volume
- 3
- Issue
- 4
- Pages
- 325-337
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W2088152552
- Cited by
- 291
- References
- 10
- FWCI
- 19.90
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Presenilin Proteins Undergo Heterogeneous Endoproteolysis between Thr291and Ala299and Occur as Stable N- and C-Terminal Fragments in Normal and Alzheimer Brain Tissue. https://app.cochat.ai/papers/10.1006/nbdi.1997.0129
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- Podlisny, M. B., Citron, M., Amarante, P., Sherrington, R., Xia, W., Zhang, J., Diehl, T., Levesque, G., Fraser, P., Haass, C., Koo, E. H. M., Seubert, P., St. George-Hyslop, P., Teplow, D. B., & Selkoe, D. J. (1997). Presenilin Proteins Undergo Heterogeneous Endoproteolysis between Thr291and Ala299and Occur as Stable N- and C-Terminal Fragments in Normal and Alzheimer Brain Tissue. Neurobiology of Disease. https://doi.org/10.1006/nbdi.1997.0129
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
