Evidence map›Paper›PMID 39062522›Full record

ArticleBiomolecules2024

DNA Base Damage Repair Crosstalks with Chromatin Structures to Contract Expanded GAA Repeats in Friedreich's Ataxia.

Yanhao Lai, Nicole Diaz, Rhyisa Armbrister, Irina Agoulnik, Yuan Liu

Abstract read
In one paragraph

Article in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Yanhao LaiDepartment of Chemistry and Biochemistry, Florida International University, 11200 SW 8th Street, Miami, FL 33199, USA.
Nicole DiazDepartment of Chemistry and Biochemistry, Florida International University, 11200 SW 8th Street, Miami, FL 33199, USA.
Rhyisa ArmbristerBiochemistry Ph.D. Program, Florida International University, 11200 SW 8th Street, Miami, FL 33199, USA.ORCID 0000-0001-6595-7020
Irina AgoulnikBiochemistry Ph.D. Program, Florida International University, 11200 SW 8th Street, Miami, FL 33199, USA.
Yuan LiuDepartment of Chemistry and Biochemistry, Florida International University, 11200 SW 8th Street, Miami, FL 33199, USA.

Funding

Frataxin Gene-Targeted GAA Repeat Contraction Through A Vault Bionanoparticle-Mediated CRISPR/dCas9 System In Friedreich's AtaxiaR03NS132097 · NINDS · FLORIDA INTERNATIONAL UNIVERSITY · PI LIU, YUAN · 2023 to 2024
$265k
NIH HHS NS132097NINDS NIH HHS R03 NS132097
6 · The paper itself

Abstract

Trinucleotide repeat (TNR) expansion is the cause of over 40 neurodegenerative diseases, including Huntington's disease and Friedreich's ataxia (FRDA). There are no effective treatments for these diseases due to the poor understanding of molecular mechanisms underlying somatic TNR expansion and contraction in neural systems. We and others have found that DNA base excision repair (BER) actively modulates TNR instability, shedding light on the development of effective treatments for the diseases by contracting expanded repeats through DNA repair. In this study, temozolomide (TMZ) was employed as a model DNA base damaging agent to reveal the mechanisms of the BER pathway in modulating GAA repeat instability at the frataxin (

Indexed as

ChromatinDNA RepairFrataxinFriedreich AtaxiaIron-Binding ProteinsMice, TransgenicTrinucleotide Repeat ExpansionAnimalsDNA DamageDNA Polymerase betaHumansMiceNeuronsTemozolomideChromatinDNA Polymerase betaFrataxinIron-Binding ProteinsTemozolomidebase excision repairFriedreich’s ataxiainhibition of histone H3K9 methylationrepeat contractiontrinucleotide

Identifiers

PMID39062522
PMCPMC11274795

What OpenQuestion holds

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Registered trials

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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.