Evidence map›Paper›PMID 35444517›Full record

ReviewFrontiers in cellular neuroscience2022

Polyglutamine Expansion in Huntingtin and Mechanism of DNA Damage Repair Defects in Huntington's Disease.

Subrata Pradhan, Rui Gao, Keegan Bush, Nan Zhang, Yogesh P Wairkar, Partha S Sarkar

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

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  10. mEMBO reports · 2024
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  18. Nuclear Pore Dysfunction in Neurodegeneration.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    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

6 authors at 2 institutions in 1 country.

Subrata PradhanDepartment of Neurology, University of Texas Medical Branch, Galveston, TX, United States.
Rui GaoDepartment of Neurology, University of Texas Medical Branch, Galveston, TX, United States.
Keegan BushDepartment of Neuroscience, Cell Biology and Anatomy, University of Texas Medical Branch, Galveston, TX, United States.
Nan ZhangDepartment of Neurology, Houston Methodist Research Institute, Houston, TX, United States.
Yogesh P WairkarDepartment of Neurology, University of Texas Medical Branch, Galveston, TX, United States.
Partha S SarkarDepartment of Neurology, University of Texas Medical Branch, Galveston, TX, United States.
The University of Texas Medical Branch at Galveston · USHouston Methodist · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence suggests that DNA repair deficiency and genome instability may be the impending signs of many neurological diseases. Genome-wide association (GWAS) studies have established a strong correlation between genes that play a role in DNA damage repair and many neurodegenerative diseases, including Huntington's disease (HD), and several other trinucleotides repeat expansion-related hereditary ataxias. Recently, many reports have documented a significant role played by the DNA repair processes in aging and in modifying many neurodegenerative diseases, early during their progression. Studies from our lab and others have now begun to understand the mechanisms that cause defective DNA repair in HD and surprisingly, many proteins that have a strong link to known neurodegenerative diseases seem to be important players in these cellular pathways. Mutations in

Indexed as

defective DNA damage repairhuntingtinHuntington’s diseasemicrosatellite repeat expansionpolyglutamine repeat expansiontranscription-coupled DNA repair

Identifiers

PMID35444517
PMCPMC9013776
OpenAlexW4226053942

What OpenQuestion holds

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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.