Evidence map›Paper›PMID 40361117›Full record

ArticleCell communication and signaling : CCS2025

RYBP promotes HIV-1 latency through promoting H2AK119ub and decreasing H3K4me3.

Xinyi Yang, Yuqi Zhu, Xiaying Zhao, Jingna Xun, Xingyu Wang, Yipeng Cheng, Su Xiong, Xingwen Yu, Suixiang Li, Danqing Wang and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 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

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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. 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

16 authors.

Xinyi Yang *State Key Laboratory of Genetic Engineering and Engineering Research Center of Gene Technology, Ministry of Education, Institute of Genetics, School of Life Sciences, Yiwu Research Institute of Fudan University, Fudan University, Shanghai, China. xinyy@fudan.edu.cn.
Yuqi Zhu *State Key Laboratory of Genetic Engineering and Engineering Research Center of Gene Technology, Ministry of Education, Institute of Genetics, School of Life Sciences, Yiwu Research Institute of Fudan University, Fudan University, Shanghai, China.
Xiaying Zhao *State Key Laboratory of Genetic Engineering and Engineering Research Center of Gene Technology, Ministry of Education, Institute of Genetics, School of Life Sciences, Yiwu Research Institute of Fudan University, Fudan University, Shanghai, China.
Jingna XunState Key Laboratory of Genetic Engineering and Engineering Research Center of Gene Technology, Ministry of Education, Institute of Genetics, School of Life Sciences, Yiwu Research Institute of Fudan University, Fudan University, Shanghai, China.
Xingyu WangState Key Laboratory of Genetic Engineering and Engineering Research Center of Gene Technology, Ministry of Education, Institute of Genetics, School of Life Sciences, Yiwu Research Institute of Fudan University, Fudan University, Shanghai, China.
Yipeng ChengState Key Laboratory of Genetic Engineering and Engineering Research Center of Gene Technology, Ministry of Education, Institute of Genetics, School of Life Sciences, Yiwu Research Institute of Fudan University, Fudan University, Shanghai, China.
Su XiongState Key Laboratory of Genetic Engineering and Engineering Research Center of Gene Technology, Ministry of Education, Institute of Genetics, School of Life Sciences, Yiwu Research Institute of Fudan University, Fudan University, Shanghai, China.
Xingwen YuState Key Laboratory of Genetic Engineering and Engineering Research Center of Gene Technology, Ministry of Education, Institute of Genetics, School of Life Sciences, Yiwu Research Institute of Fudan University, Fudan University, Shanghai, China.
Suixiang LiState Key Laboratory of Genetic Engineering and Engineering Research Center of Gene Technology, Ministry of Education, Institute of Genetics, School of Life Sciences, Yiwu Research Institute of Fudan University, Fudan University, Shanghai, China.
Danqing WangYunnan Provincial Infectious Diseases Hospital/Yunnan AIDS Care Center, Kunming, China.
Zhiliang HuDepartment of Infectious Disease, The Second Hospital of Nanjing, Nanjing University of Chinese Medicine, Nanjing Medical University, Center for Global Health, School of Public Health, Nanjing, China.
Yinzhong ShenScientific Research Center, Shanghai Public Health Clinical Center, Fudan University, Shanghai, China.
Shibo JiangKey Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), Shanghai Institute of Infectious Disease and Biosecurity, School of Basic Medical Sciences, Fudan University, Shanghai, China.
Hongzhou LuDepartment of Infectious Diseases and Nursing Research Institution, National Clinical Research Center for Infectious Diseases, The Third People's Hospital of Shenzhen, Shenzhen, Guangdong, China.
Gang WangState Key Laboratory of Genetic Engineering and Engineering Research Center of Gene Technology, Ministry of Education, Institute of Genetics, School of Life Sciences, Yiwu Research Institute of Fudan University, Fudan University, Shanghai, China.
Huanzhang ZhuState Key Laboratory of Genetic Engineering and Engineering Research Center of Gene Technology, Ministry of Education, Institute of Genetics, School of Life Sciences, Yiwu Research Institute of Fudan University, Fudan University, Shanghai, China. hzzhu@fudan.edu.cn.

Funding

National Key Research and Development Program of China 2023YFC2306700National Key Research and Development Program of China 2024YFC2300110National Natural Science Foundation of China 82402609
6 · The paper itself

Abstract

backgroundAcquired immunodeficiency syndrome (AIDS) cannot be completely cured, and the main obstacle is the existence of viral reservoirs. However, we currently do not fully understand the molecular mechanisms by which HIV-1 latency is established and maintained.

methodsHere, based on engineered chromatin immunoprecipitation (enChIP) technology that using FLAG-tagged zinc finger nucleic acid proteins (FLAG-ZFP) that bind to the HIV-1 L region and chromatin immunoprecipitation, we identified RYBP as a new HIV-1 latency-promoting gene. The effect of RYBP on HIV-1 latency was explored in multiple cell lines and primary latency models through gene knockout methods. Western blot and chromatin immunoprecipitation (ChIP) were used to explore the molecular mechanism of RYBP in promoting HIV-1 latency.

resultsDisruption of RYBP gene can activate latent HIV-1 in different latent cell lines and primary latent cell models. Mechanistically, the HIV-1 long terminal repeats (LTR) region binding protein Yin Yang 1 (YY1) can recruit RYBP to the HIV-1 L region. Then, RYBP can further recruit KDM2B, thereby promoting the increased ubiquitination level of H2AK119 and decreases the level of H3K4me3, to decrease HIV-1 L transcriptional elongation and enter a latent state. At the same time, during the stage of viral transcription and replication, Tat protein can inhibit the expression of RYBP, promoting viral transcription and replication. Finally, we found that the H2AK119ub inhibitor PRT4165 can promote latent HIV-1 activation and has good synergy with reported latent reactivating agents.

conclusionThese results provide mechanistically new insights into a critical role of RYBP in the regulation of histone modification and H2AK119ub may be directly targeted to control HIV reservoirs.

Indexed as

HistonesHIV-1Repressor ProteinsVirus LatencyHEK293 CellsHumansUbiquitinationhistone H3 trimethyl Lys4HistonesRepressor ProteinsEnChIPH2AK119ubHIV-1 latencyKDM2BRYBP

Identifiers

PMID40361117
PMCPMC12070685

What OpenQuestion holds

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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.