CoChat
Sign Up
Cited by 11

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

A novel beta-site amyloid precursor protein cleaving enzyme (BACE) isoform regulated by nonsense-mediated mRNA decay and proteasome-dependent degradation

Tanahashi, Hiroshi, Tabira, Takeshi·2007·Neuroscience Letters
DOI 10.1016/j.neulet.2007.09.033
Open this paper in CoChat — free account

Abstract

Proteolytic cleavage of amyloid beta-peptide (Abeta) from amyloid precursor protein (APP) is a key event in the pathogenesis of Alzheimer's disease. Beta-site amyloid precursor protein cleaving enzyme (BACE) cleaves the APP at the N-terminus of Abeta. We investigated whether particular stress conditions modify the expression and activity of BACE, and found that treatment of human neuroblastoma cells with protein synthesis inhibitors induced expression of a novel splice variant of BACE. This unusual transcript, I-127, is produced by usage of an internal splicing donor site in exon 3. The splicing event leads to a premature termination codon, as well as elimination of one of two conserved aspartic protease active sites, a transmembrane domain, and a C-terminal cytoplasmic tail from BACE. Low levels of this mRNA were found in the human brain. When expressed in cells, I-127 had no effect on Abeta secretion and was retained in the endoplasmic reticulum without propeptide removal. It was also unstable with a turnover t(1/2) of approximately 2h; normal BACE had a turnover t(1/2) of approximately 8h. Finally, I-127 was degraded in a proteasome-dependent manner. Thus, I-127 is regulated by both nonsense-mediated mRNA decay (NMD) and proteasome-dependent degradation.

Overview

Integrity signals

Registry

Crossref · 10.1016/j.neulet.2007.09.033

Cites

1 of 1 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • There are six relatively established BACE1 isoforms (A-F), in addition to reports of various less well-characterized forms including BACE1-455 and BACE1-127.

    “There are six relatively established BACE1 isoforms (A–F), in addition to reports of various less well‐characterized forms including BACE1‐455 and BACE1‐127”

    From BACE1: More than just a β‐secretase (2022) · cites this paper as [69]

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 17

  1. Bodendorf, 2001, A splice variant of β-secretase deficient in the amyloidogenic processing of the amyloid precursor protein, J. Biol. Chem., 276, 12019, 10.1074/jbc.M008861200 · DOI · Paper page
  2. Capell, 2000, Maturation and pro-peptide cleavage of beta-secretase, J. Biol. Chem., 275, 30849, 10.1074/jbc.M003202200 · DOI · Paper page
  3. Ehehalt, 2002, Splice variants of the β-site APP-cleaving enzyme BACE1 in human brain and pancreas, Biochem. Biophys. Res. Commun., 293, 30, 10.1016/S0006-291X(02)00169-9 · DOI · Paper page
  4. Haniu, 2000, Characterization of Alzheimer's beta-secretase protein BACE. A pepsin family member with unusual properties, J. Biol. Chem., 275, 21099, 10.1074/jbc.M002095200 · DOI
  5. Hol, 2003, Neuronal expression of GFAP in patients with Alzheimer pathology and identification of novel GFAP splice form, Mol. Psychiatry, 8, 786, 10.1038/sj.mp.4001379 · DOI
  6. Huse, 2000, Maturation and endosomal targeting of β-site amyloid precursor protein-cleaving enzyme: the Alzheimer's disease beta-secretase, J. Biol. Chem., 275, 33729, 10.1074/jbc.M004175200 · DOI · Paper page
  7. Keck, 2003, Proteasome inhibition by paired helical filament-tau in brains of patients with Alzheimer's disease, J. Neurochem., 75, 115, 10.1046/j.1471-4159.2003.01642.x · DOI · Paper page
  8. Keller, 2000, Impaired proteasome function in Alzheimer's disease, J. Neurochem., 75, 436, 10.1046/j.1471-4159.2000.0750436.x · DOI · Paper page
  9. Khajavi, 2006, Nonsense-mediated mRNA decay modulates clinical outcome of genetic disease, Eur. J. Hum. Genet., 14, 1074, 10.1038/sj.ejhg.5201649 · DOI
  10. Lewis, 2003, Evidence for the widespread coupling of alternative splicing and nonsense-mediated mRNA decay in humans, Proc. Natl. Acad. Sci. U.S.A., 100, 189, 10.1073/pnas.0136770100 · DOI
  11. Majoul, 1996, Transport of an external Lys-Asp-Glu-Leu (KDEL) protein from the plasma membrane to the endoplasmic reticulum: Studies with cholera toxin in Vero cells, J. Cell Biol., 133, 777, 10.1083/jcb.133.4.777 · DOI
  12. Molinari, 2002, Sequential assistance of molecular chaperones and transient formation of covalent complexes during protein degradation from ER, J. Cell Biol., 158, 247, 10.1083/jcb.200204122 · DOI
  13. Sato, 1999, A novel presenilin-2 splice variant in human Alzheimer's disease brain tissue, J Neurochem., 72, 2498, 10.1046/j.1471-4159.1999.0722498.x · DOI
  14. Suzuki, 1994, An increased percentage of long amyloid beta protein secreted by familial amyloid beta protein precursor (beta APP717) mutants, Science, 264, 1336, 10.1126/science.8191290 · DOI · Paper page
  15. Tanahashi, 2001, Three novel alternatively spliced isoforms of the human beta-site amyloid precursor protein cleaving enzyme (BACE) and their effect on amyloid beta-peptide production, Neurosci. Lett., 307, 9, 10.1016/S0304-3940(01)01912-7 · DOI · Paper page
  16. van Leeuwen, 1998, Frameshift mutats of β amyloide precursor protein and ubiquitin-B in Alzheimer's and Down patients, Science, 279, 242, 10.1126/science.279.5348.242 · DOI
  17. Vassar, 2001, The beta-secretase, BACE: a prime drug target for Alzheimer's disease, J. Mol. Neurosci., 17, 157, 10.1385/JMN:17:2:157 · DOI

Cited by

Sorted by citations

Metadata

Authors
Tanahashi, H., & Tabira, T.
Venue
Neuroscience Letters
Publisher
Elsevier BV
Published
2007-11
Volume
428
Issue
2-3
Pages
103-108
ISSN
0304-3940
DOI
10.1016/j.neulet.2007.09.033
Cited by
11
References
1
Language
en
Licence

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review