Evidence map›Paper›PMID 27649271›Full record

ArticleBiochemistry2016

Transmembrane Substrate Determinants for γ-Secretase Processing of APP CTFβ.

Marty A Fernandez, Kelly M Biette, Georgia Dolios, Divya Seth, Rong Wang, Michael S Wolfe

Abstract read
In one paragraph

Article in Biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.3field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Amyloidogenesis: What Do We Know So Far?International journal of molecular sciences · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Marty A FernandezAnn Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School , Boston, Massachusetts 02115, United States.
Kelly M BietteAnn Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School , Boston, Massachusetts 02115, United States.
Georgia DoliosIcahn School of Medicine at Mount Sinai , New York, New York 10029, United States.
Divya SethAnn Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School , Boston, Massachusetts 02115, United States.
Rong WangIcahn School of Medicine at Mount Sinai , New York, New York 10029, United States.
Michael S WolfeAnn Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School , Boston, Massachusetts 02115, United States.
Harvard University · USIcahn School of Medicine at Mount Sinai · USBrigham and Women's Hospital · US

Funding

THE NINDS MASS SPECTROMETRY PROTEOMICS CENTER FOR NEUROSCIENCES AT MSSMP30NS061777 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI WANG, RONG · 2009 to 2014
$3.9M
Trimming of Amyloid Peptides by Gamma-SecretaseR03NS081498 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI WOLFE, MICHAEL S · 2012 to 2013
$173k
NINDS NIH HHS P30 NS061777NINDS NIH HHS R03 NS081498
6 · The paper itself

Abstract

The amyloid β-peptide (Aβ) of Alzheimer's disease (AD) is generated by proteolysis within the transmembrane domain (TMD) of a C-terminal fragment of the amyloid β protein-precursor (APP CTFβ) by the γ-secretase complex. This processing produces Aβ ranging from 38 to 49 residues in length. Evidence suggests that this spectrum of Aβ peptides is the result of successive γ-secretase cleavages, with endoproteolysis first occurring at the ε sites to generate Aβ48 or Aβ49, followed by C-terminal trimming mostly every three residues along two product lines to generate shorter, secreted forms of Aβ: the primary Aβ49-46-43-40 line and a minor Aβ48-45-42-38 line. The major secreted Aβ species are Aβ40 and Aβ42, and an increased proportion of the longer, aggregation-prone Aβ42 compared to Aβ40 is widely thought to be important in AD pathogenesis. We examined TMD substrate determinants of the specificity and efficiency of ε site endoproteolysis and carboxypeptidase trimming of CTFβ by γ-secretase. We determined that the C-terminal negative charge of the intermediate Aβ49 does not play a role in its trimming by γ-secretase. Peptidomimetic probes suggest that γ-secretase has S1', S2', and S3' pockets, through which trimming by tripeptides may be determined. However, deletion of residues around the ε sites demonstrates that a depth of three residues within the TMD is not a determinant of the location of endoproteolytic ε cleavage of CTFβ. We also show that instability of the CTFβ TMD helix near the ε site significantly increases endoproteolysis, and that helical instability near the carboxypeptidase cleavage sites facilitates C-terminal trimming by γ-secretase. In addition, we found that CTFβ dimers are not endoproteolyzed by γ-secretase. These results support a model in which initial interaction of the array of residues along the undimerized single helical TMD of substrates dictates the site of initial ε cleavage and that helix unwinding is essential for both endoproteolysis and carboxypeptidase trimming.

Indexed as

Amyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesProtein Processing, Post-TranslationalSubstrate SpecificityAmyloid beta-Protein PrecursorAmyloid Precursor Protein Secretases

Identifiers

PMID27649271
PMCPMC5539764
OpenAlexW2524674947

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.