Evidence map›Paper›PMID 19699304›Full record

ArticleNeurobiology of disease2009

Disruption of Rab11 activity in a knock-in mouse model of Huntington's disease.

Xueyi Li, Ellen Sapp, Kathryn Chase, Laryssa A Comer-Tierney, Nicholas Masso, Jonathan Alexander, Patrick Reeves, Kimberly B Kegel, Antonio Valencia, Miguel Esteves and 2 more

Abstract readComparative Study
In one paragraph

Article in Neurobiology of disease, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
–field-weighted citation impact
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

46 citing papers in PubMed.

  1. Review
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  6. Endo-lysosomal dysfunction in neurodegenerative diseases: opinion on current progress and future direction in the use of exosomes as biomarkers.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Review
  7. Review
  8. Article
  9. Article
  10. Review
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  15. Vps54 regulatesBiology open · 2020
    Article
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  17. Review
  18. Review
  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

12 authors.

Xueyi LiDepartment of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA. xli12@partners.org
Ellen Sapp
Kathryn Chase
Laryssa A Comer-Tierney
Nicholas Masso
Jonathan Alexander
Patrick Reeves
Kimberly B Kegel
Antonio Valencia
Miguel Esteves
Neil Aronin
Marian Difiglia

Funding

SIGNALING MECHANISMS IN NEURONAL DEGENERATIONR01NS038194 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI ARONIN, NEIL · 1999 to 2014
$6.2M
Role of Huntingtin in Vesicle TransportR01NS035711 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI DIFIGLIA, MARIAN · 1998 to 2005
$3.0M
NINDS NIH HHS NS35711NINDS NIH HHS NS38194NINDS NIH HHS R01 NS035711NINDS NIH HHS R01 NS038194
6 · The paper itself

Abstract

The Huntington's disease (HD) mutation causes polyglutamine expansion in huntingtin (Htt) and neurodegeneration. Htt interacts with a complex containing Rab11GDP and is involved in activation of Rab11, which functions in endosomal recycling and neurite growth and long-term potentiation. Like other Rab proteins, Rab11GDP undergoes nucleotide exchange to Rab11GTP for its activation. Here we show that striatal membranes of HD(140Q/140Q) knock-in mice are impaired in supporting conversion of Rab11GDP to Rab11GTP. Dominant negative Rab11 expressed in the striatum and cortex of normal mice caused neuropathology and motor dysfunction, suggesting that a deficiency in Rab11 activity is pathogenic in vivo. Primary cortical neurons from HD(140Q/140Q) mice were delayed in recycling transferrin receptors back to the plasma membrane. Partial rescue from glutamate-induced cell death occurred in HD neurons expressing dominant active Rab11. We propose a novel mechanism of HD pathogenesis arising from diminished Rab11 activity at recycling endosomes.

Indexed as

Disease Models, AnimalGene Knock-In TechniquesAnimalsCell CycleCell LineCells, CulturedEndosomesGene Expression RegulationHuntington DiseaseMiceMice, Neurologic Mutantsrab11 GTP-Binding Proteinsrab GTP-Binding Proteinsrab11 GTP-Binding Proteinsrab GTP-Binding Proteins

Identifiers

PMID19699304
PMCPMC2798579

What OpenQuestion holds

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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.