Evidence map›Paper›PMID 34098113›Full record

ReviewAgeing research reviews2021

Gene targeting techniques for Huntington's disease.

Eric Fields, Erik Vaughan, Deepika Tripu, Isabelle Lim, Katherine Shrout, Jessica Conway, Nicole Salib, Yubin Lee, Akash Dhamsania, Michael Jacobsen and 3 more

Open access · hybridAbstract readReview
In one paragraph

Review in Ageing research reviews, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

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  11. The genetic architecture of fibromyalgia across 2.5 million individuals.medRxiv : the preprint server for health sciences · 2025
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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

13 authors at 1 institution in 1 country.

Eric FieldsGemstone Honors Program, University of Maryland, College Park, MD 20742, United States.
Erik VaughanGemstone Honors Program, University of Maryland, College Park, MD 20742, United States.
Deepika TripuGemstone Honors Program, University of Maryland, College Park, MD 20742, United States.
Isabelle LimGemstone Honors Program, University of Maryland, College Park, MD 20742, United States.
Katherine ShroutGemstone Honors Program, University of Maryland, College Park, MD 20742, United States.
Jessica ConwayGemstone Honors Program, University of Maryland, College Park, MD 20742, United States.
Nicole SalibGemstone Honors Program, University of Maryland, College Park, MD 20742, United States.
Yubin LeeGemstone Honors Program, University of Maryland, College Park, MD 20742, United States.
Akash DhamsaniaGemstone Honors Program, University of Maryland, College Park, MD 20742, United States.
Michael JacobsenGemstone Honors Program, University of Maryland, College Park, MD 20742, United States.
Ashley WooGemstone Honors Program, University of Maryland, College Park, MD 20742, United States.
Huijing XueDepartment of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742, United States.
Kan CaoGemstone Honors Program, University of Maryland, College Park, MD 20742, United States; Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742, United States. Electronic address: kcao@umd.edu.
University of Maryland, College Park · US

Funding

Investigation of smooth muscle cell loss in progeriaR01HL126784 · NHLBI · UNIV OF MARYLAND, COLLEGE PARK · PI CAO, KAN · 2016 to 2020
$2.1M
NHLBI NIH HHS R01 HL126784
6 · The paper itself

Abstract

Huntington's disease (HD) is an autosomal neurodegenerative disorder caused by extended trinucleotide CAG repetition in the HTT gene. Wild-type huntingtin protein (HTT) is essential, involved in a variety of crucial cellular functions such as vesicle transportation, cell division, transcription regulation, autophagy, and tissue maintenance. The mutant HTT (mHTT) proteins in the body interfere with HTT's normal cellular functions and cause additional detrimental effects. In this review, we discuss multiple approaches targeting DNA and RNA to reduce mHTT expression. These approaches are categorized into non-allele-specific silencing and allele-specific-silencing using Single Nucleotide Polymorphisms (SNPs) and haplogroup analysis. Additionally, this review discusses a potential application of recent CRISPR prime editing technology in targeting HD.

Indexed as

Huntington DiseaseAllelesGene Expression RegulationGene TargetingHumansHuntingtin ProteinHuntingtin ProteinAllele-specific targetingHuntington’s diseasePrime editingSNPs

Identifiers

PMID34098113
PMCPMC8373677
OpenAlexW3172816545

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.