Evidence map›Paper›PMID 40411394›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

IncRNA-ZFAS1, an Emerging Gate-Keeper in DNA Damage-Dependent Transcriptional Regulation.

Jiena Liu, Qing Lu, Zixuan Fan, Jiahui Lin, Nan He, Xin Zhang, Zhaoya Han, Tingting Zhu, Zhenzhen Wu, Yingying Xu and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. IncRNA-ZFAS1, an Emerging Gate-Keeper in DNA Damage-Dependent Transcriptional Regulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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

11 authors.

Jiena LiuDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, P. R. China.
Qing LuDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, P. R. China.
Zixuan FanDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, P. R. China.
Jiahui LinDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, P. R. China.
Nan HeSchool of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, 510515, P. R. China.
Xin ZhangDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, P. R. China.
Zhaoya HanDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, P. R. China.
Tingting ZhuDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, P. R. China.
Zhenzhen WuDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, P. R. China.
Yingying XuDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, P. R. China.
Yuming WangDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, 511436, P. R. China.ORCID https://orcid.org/0000-0003-4644-4013

Funding

GuangDong Basic and Applied Basic Research Foundation 2024A1515010263National Natural Science Foundation of China 32100435National Natural Science Foundation of China 82271195
6 · The paper itself

Abstract

Numerous long noncoding RNAs (lncRNAs) are generated in response to external stimuli, but the scope and functions of such activity are not known. Here, this study provides insight into how the transcription of lncRNAs is connected to DNA damage response by identifying the lncRNA ZFAS1, which is required for cell cycle arrest, transcription regulation, and DNA repair. Mechanistically, ZFAS1 facilitates dynamic changes in hyperphosphorylated forms of the large subunit of RNA polymerase II (RNAPII) around transcription initiation sites by directly targeting the regulated genes. It is shown that extensive transcription shutdown and concomitant stimulated engagement of RNAPII-Ser2P are crucial for repair and cell survival upon genotoxic stress. Finally, ZFAS1 knockout in mice dampened nucleotide excision repair (NER) and led to kidney dysplasia. Overall, the findings extend the understanding of lncRNAs in DNA damage repair (DDR) and imply a protective role of lncRNA against DDR-deficient developmental disorders.

Indexed as

DNA DamageGene Expression RegulationRNA, Long NoncodingTranscription, GeneticAnimalsDNA RepairHumansMiceMice, KnockoutRNA Polymerase IIRNA, Long NoncodingRNA Polymerase IIIncRNA‐ZFAS1nucleotide excision repairtranscription regulationUV‐C irradiation

Identifiers

PMID40411394
PMCPMC12376587

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.