Evidence map›Paper›PMID 21605032›Full record

ReviewCurrent Alzheimer research2012

An overview of notch signaling in adult tissue renewal and maintenance.

Chihiro Sato, Guojun Zhao, Ma Xenia G Ilagan

Abstract readReview
In one paragraph

Review in Current Alzheimer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

35 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Notch Signaling in Acute Inflammation and Sepsis.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Biochemistry and biophysics reports · 2021
    Article
  17. Article
  18. Ethyl Pyruvate-Derived Transdifferentiation of Astrocytes to Oligodendrogenesis in Cuprizone-Induced Demyelinating Model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Article
  19. Article
  20. Notch Signaling Regulation in Autoinflammatory Diseases.International journal of molecular sciences · 2020
    Review
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

3 authors at 1 institution in 1 country.

Chihiro SatoDepartment of Developmental Biology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Guojun Zhao
Ma Xenia G Ilagan
Washington University in St. Louis · US

Funding

WASHINGTON UNIVERSITY ALZHEIMERS DISEASE RESEARCH CENTERP50AG005681 · NIA · WASHINGTON UNIVERSITY · PI MORRIS, JOHN · 1985 to 2019
$52.1M
BIOCHEMICAL AND GENETIC ANALYSIS OF NOTCH SIGNALINGR01GM055479 · NIGMS · WASHINGTON UNIVERSITY · PI KOPAN, RAPHAEL, WEIRAUCH, MATTHEW TYSON · 1996 to 2021
$6.4M
Mapping substrate/gamma-secretase interactionsR01AG025973 · NIA · WASHINGTON UNIVERSITY · PI KOPAN, RAPHAEL · 2005 to 2009
$1.5M
NIA NIH HHS AG025973NIA NIH HHS P50 AG005681NIA NIH HHS P50 AG05681NIA NIH HHS R01 AG025973NIGMS NIH HHS GM55479NIGMS NIH HHS R01 GM055479
6 · The paper itself

Abstract

The Notch pathway is a critical mediator of short-range cell-cell communication that is reiteratively used to regulate a diverse array of cellular processes during embryonic development and the renewal and maintenance of adult tissues. Most Notch-dependent processes utilize a core signaling mechanism that is dependent on regulated intramembrane proteolysis: Upon ligand binding, Notch receptors undergo ectodomain shedding by ADAM metalloproteases, followed by γ-secretase-mediated intramembrane proteolysis. This releases the Notch intracellular domain, which translocates to the nucleus to activate transcription. In this review, we highlight the roles of Notch signaling particularly in self-renewing tissues in adults and several human diseases and raise some key considerations when targeting ADAMs and γ-secretase as disease-modifying strategies for Alzheimer's Disease.

Indexed as

ADAM ProteinsAmyloid Precursor Protein SecretasesAnimalsCell CommunicationHumansModels, BiologicalReceptors, NotchSignal TransductionWounds and InjuriesADAM ProteinsAmyloid Precursor Protein SecretasesReceptors, Notch

Identifiers

PMID21605032
PMCPMC4361071
OpenAlexW2161361170

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.