Evidence map›Paper›PMID 28954224›Full record

ArticleCell reports2017

Alterations in mRNA 3' UTR Isoform Abundance Accompany Gene Expression Changes in Human Huntington's Disease Brains.

Lindsay Romo, Ami Ashar-Patel, Edith Pfister, Neil Aronin

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Regulation ofInternational journal of molecular sciences · 2024
    Review
  4. Article
  5. Regulatory features aid interpretation of 3'UTR variants.American journal of human genetics · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. RNA Modifications and RNA Metabolism in Neurological Disease Pathogenesis.International journal of molecular sciences · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. Emerging Roles for 3' UTRs in Neurons.International journal of molecular sciences · 2020
    Review
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Lindsay RomoDepartment of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. Electronic address: lindsay.romo@umassmed.edu.
Ami Ashar-PatelRNA Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Edith PfisterDepartment of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Neil AroninDepartment of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA; RNA Therapeutics Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. Electronic address: neil.aronin@umassmed.edu.
University of Massachusetts Chan Medical School · US

Funding

SIGNALING MECHANISMS IN NEURONAL DEGENERATIONR01NS038194 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ARONIN, NEIL · 1999 to 2014
$6.2M
Investigating the Mechanism and Effect of Disease-Associated Increases in the Huntingtin Long 3'UTR IsoformF30NS095450 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ROMO, LINDSAY SARA · 2015 to 2018
$116k
NINDS NIH HHS F30 NS095450NINDS NIH HHS R01 NS038194
6 · The paper itself

Abstract

The huntingtin gene has two mRNA isoforms that differ in their 3' UTR length. The relationship of these isoforms with Huntington's disease is not established. We provide evidence that the abundance of huntingtin 3' UTR isoforms differs between patient and control neural stem cells, fibroblasts, motor cortex, and cerebellum. Huntingtin 3' UTR isoforms, including a mid-3' UTR isoform, have different localizations, half-lives, polyA tail lengths, microRNA sites, and RNA-binding protein sites. Isoform shifts in Huntington's disease motor cortex are not limited to huntingtin; 11% of alternatively polyadenylated genes change the abundance of their 3' UTR isoforms. Altered expression of RNA-binding proteins may be associated with aberrant isoform abundance; knockdown of the RNA-binding protein CNOT6 in control fibroblasts leads to huntingtin isoform differences similar to those in disease fibroblasts. These findings demonstrate that mRNA 3' UTR isoform changes are a feature of molecular pathology in the Huntington's disease brain.

Indexed as

3' Untranslated RegionsAnimalsBrainHumansHuntington DiseaseMiceNuclear ProteinsProtein IsoformsRNA, Messenger3' Untranslated RegionsNuclear ProteinsProtein IsoformsRNA, Messenger3′ UTR isoformsalternative polyadenylationhuntingtinHuntington’s diseasepolyA site sequencing

Identifiers

PMID28954224
PMCPMC5625827
OpenAlexW2758599721

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.