Evidence map›Paper›PMID 23829302›Full record

ReviewThe FEBS journal2013

Genetic manipulations of mutant huntingtin in mice: new insights into Huntington's disease pathogenesis.

C Y Daniel Lee, Jeffrey P Cantle, X William Yang

Open access · bronzeAbstract readReview
In one paragraph

Review in The FEBS journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Pain in Huntington's disease and its potential mechanisms.Frontiers in aging neuroscience · 2023
    Review
  5. Article
  6. Review
  7. Synaptic Dysfunction in Huntington's Disease: Lessons from Genetic Animal Models.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. The Role of Adenosine Tone and Adenosine Receptors in Huntington's Disease.Journal of caffeine and adenosine research · 2018
    Review
  18. Review
  19. Mutant Huntingtin Inhibits αB-Crystallin Expression and Impairs Exosome Secretion from Astrocytes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  20. Huntington's Disease: Mechanisms of Pathogenesis and Therapeutic Strategies.Cold Spring Harbor perspectives in medicine · 2017
    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 2 institutions in 1 country.

C Y Daniel LeeCenter for Neurobehavioral Genetics, Semel Institute for Neuroscience and Human Behaviors, David Geffen School of Medicine at University of California, Los Angeles, CA 90095, USA.
Jeffrey P Cantle
X William Yang
Neurobehavioral Systems · USUniversity of California, Los Angeles · US

Funding

Conditional Mouse Models: Non-cell-antonomous Toxicities in Huntington's DiseaseR01NS049501 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YANG, XIANGDONG WILLIAM · 2004 to 2014
$3.8M
Validating NT17 Dependent Mechanisms in Huntington's Disease SuppressionR01NS074312 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YANG, XIANGDONG WILLIAM · 2011 to 2014
$1.4M
NINDS NIH HHS R01 NS049501NINDS NIH HHS R01NS049501NINDS NIH HHS R01 NS074312NINDS NIH HHS R01NS074312
6 · The paper itself

Abstract

This year (2013) marks the 20th anniversary of identification of the causal genetic mutation for Huntington's disease (HD), a landmark discovery that heralded study of the biological underpinnings of this most common dominantly inherited neurodegenerative disorder. Among the variety of model organisms used to study HD pathogenesis, the mouse model is by far the most commonly used mammalian genetic model. Much of our current knowledge regarding mutant huntingtin (mHtt)-induced disease pathogenesis in mammalian models has been obtained by studying transgenic mouse models expressing mHtt N-terminal fragments, full-length murine or human mHtt. In this review, we focus on recent progress in using novel HD mouse models with targeted mHtt expression in specific brain cell types. These models help to address the role of distinct neuronal and non-neuronal cell types in eliciting cell-autonomous or non-cell-autonomous disease processes in HD. We also describe several mHtt transgenic mouse models with targeted mutations in Htt cis-domains to address specific pathogenic hypotheses, ranging from mHtt proteolysis to post-translational modifications. These novel mouse genetic studies, through direct manipulations of the causal HD gene, utilize a reductionist approach to systematically unravel the cellular and molecular pathways that are targeted by mHtt in disease pathogenesis, and to potentially identify novel targets for therapy.

Indexed as

AnimalsCaspase 6Cerebral CortexCorpus StriatumDisease Models, AnimalGene Expression RegulationHumansHuntingtin ProteinHuntington DiseaseMiceMice, TransgenicMutationNerve Tissue ProteinsNeuronsNuclear ProteinsProtein EngineeringCasp6 protein, mouseCaspase 6Htt protein, mouseHuntingtin ProteinNerve Tissue ProteinsNuclear Proteinscaspase 6cell-cell interactiongenetic manipulationgenomic transgenic miceHuntington's diseasemouse modelsnuclear translocationpost-translational modification

Identifiers

PMID23829302
PMCPMC3770892
OpenAlexW2028768867

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.