Evidence map›Paper›PMID 21985782›Full record

ArticleThe Journal of clinical investigation2011

The long and the short of aberrant ciliogenesis in Huntington disease.

Jeh-Ping Liu, Scott O Zeitlin

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 37% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Centriolar satellites: key mediators of centrosome functions.Cellular and molecular life sciences : CMLS · 2015
    Review
  9. Article
  10. Antisense therapy in neurology.Journal of personalized medicine · 2013
    Review
  11. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Jeh-Ping LiuDepartment of Neuroscience, University of Virginia, Charlottesville, Virginia, USA.
Scott O Zeitlin
University of Michigan–Ann Arbor · USUniversity of Virginia · US

Funding

Loss-of-function mechanisms in Huntington's DiseaseR01NS043466 · NINDS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI ZEITLIN, SCOTT · 2003 to 2013
$2.9M
Loss-of-function mechanisms in Huntington's diseaseR56NS043466 · NINDS · UNIVERSITY OF VIRGINIA · PI ZEITLIN, SCOTT · 2008 to 2008
$341k
NINDS NIH HHS NS043466NINDS NIH HHS R01 NS043466NINDS NIH HHS R56 NS043466
6 · The paper itself

Abstract

Huntington disease (HD) is a dominantly inherited neurodegenerative disorder that is caused by a mutant huntingtin (HTT) gene encoding a version of the Htt protein with an expanded polyglutamine stretch. Although the HTT gene was discovered more than 18 years ago, the functions of normal Htt and the mechanisms by which mutant Htt causes disease are not well defined. In this issue of the JCI, Keryer et al. uncovered a novel function for normal Htt in ciliogenesis and report that mutant Htt causes hypermorphic ciliogenesis and ciliary dysfunction. These observations suggest that it is now critical to understand the extent to which ciliary dysfunction contributes to the different symptoms of HD and to determine whether therapeutic strategies designed to normalize ciliary function can ameliorate the disease.

Indexed as

AnimalsAutoantigensCell Cycle ProteinsHumansHuntingtin ProteinHuntington DiseaseMutant ProteinsNerve Tissue ProteinsNuclear ProteinsAutoantigensCell Cycle ProteinsHAP1 protein, humanHTT protein, humanHuntingtin ProteinMutant ProteinsNerve Tissue ProteinsNuclear ProteinsPCM1 protein, human

Identifiers

PMID21985782
PMCPMC3204854
OpenAlexW1980272282

What OpenQuestion holds

Textmetadata
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.