Evidence map›Paper›PMID 24032460›Full record

ArticleJournal of neurochemistry2013

Alternative polyadenylation and miR-34 family members regulate tau expression.

John R Dickson, Carla Kruse, Daniel R Montagna, Bente Finsen, Michael S Wolfe

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neurochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 127 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. An Update on Neuroaging on Earth and in Spaceflight.International journal of molecular sciences · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. New Insights into the Roles of p53 in Central Nervous System Diseases.The international journal of neuropsychopharmacology · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. miRNAs as Therapeutic Tools in Alzheimer's Disease.International journal of molecular sciences · 2021
    Review
  20. Review

17 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 2 countries.

John R DicksonCenter for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Carla Kruse
Daniel R Montagna
Bente Finsen
Michael S Wolfe
Harvard University · USBrigham and Women's Hospital · USUniversity of Southern Denmark · DK

Funding

Training in Pharmacological SciencesT32GM007306 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI GOLAN, DAVID E. · 1985 to 2018
$6.6M
NIGMS NIH HHS GM007306NIGMS NIH HHS T32 GM007306
6 · The paper itself

Abstract

Tau pathologically aggregates in Alzheimer's disease, and evidence suggests that reducing tau expression may be safe and beneficial for the prevention or treatment of this disease. We sought to examine the role of the 3'-untranslated region (3'-UTR) of human tau mRNA in regulating tau expression. Tau expresses two 3'-UTR isoforms, long and short, as a result of alternative polyadenylation. Using luciferase reporter constructs, we found that expression from these isoforms is differentially controlled in human neuroblastoma cell lines M17D and SH-SY5Y. Several microRNAs were computationally identified as candidates that might bind the long, but not short, tau 3'-UTR isoform. A hit from a screen of candidates, miR-34a, was subsequently shown to repress the expression of endogenous tau protein in M17D cells. Conversely, inhibition of endogenously expressed miR-34 family members leads to increased endogenous tau expression. In addition, through an unbiased screen of fragments of the human tau 3'-UTR using a luciferase reporter assay, we identified several other regions in the long tau 3'-UTR isoform that contain regulatory cis-elements. Improved understanding of the regulation of tau expression by its 3'-UTR may ultimately lead to the development of novel therapeutic strategies for the treatment of Alzheimer's disease and other tauopathies. mRNA 3'-untranslated regions (3'-UTR) often regulate transcript stability or translation. Despite the centrality of the tau protein in Alzheimer's and other neurodegenerative diseases, the human tau 3'-UTR has been little studied. This report identifies regions of the tau 3'-UTR that influence expression and shows that microRNA (miR)-34a targets this 3'-UTR to lower expression, which is considered an important therapeutic goal.

Indexed as

Polyadenylation3' Untranslated RegionsBase SequenceCells, CulturedGene Expression RegulationHumansMicroRNAsMolecular Sequence DataProtein Isoformstau Proteins3' Untranslated RegionsMicroRNAsMIRN34 microRNA, humanProtein Isoformstau Proteins3′-untranslated regionAlzheimer's diseasegene regulationMAPTneurodegenerative disease

Identifiers

PMID24032460
PMCPMC3859707
OpenAlexW2002759338

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.