Evidence map›Paper›PMID 41485079›Full record

ArticleProtein & cell2026

BCL7A's arginine anchor links nucleosome recognition to chromatin remodeling and diffuse large B-cell lymphoma tumor suppression.

Jingdong Xue, Kai Tian, Xiang Xu, Yuqian Feng, Ming Yu, Min Hao, Mingqian Hu, Wenhan Wang, Jiao Ma, Yixuan Pan and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Protein & cell, 2026. 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. Structure and molecular function of the BCL7 proteins.Biochemical Society transactions · 2026
    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

18 authors.

Jingdong XueDepartment of Biochemistry and Molecular Cell Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Kai TianDepartment of Orthopedic Oncology, Shanghai Bone Tumor Institute, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Xiang XuDepartment of Laboratory Medicine, Jiading Branch of Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Yuqian FengDepartment of Biochemistry and Molecular Cell Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Ming YuDepartment of Biochemistry and Molecular Cell Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Min HaoDepartment of Biochemistry and Molecular Cell Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Mingqian HuDepartment of Biochemistry and Molecular Cell Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Wenhan WangDepartment of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Jiao MaDepartment of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Yixuan PanDepartment of Biochemistry and Molecular Cell Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Mengyuan PengDepartment of Biochemistry and Molecular Cell Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Jun WuDepartment of Laboratory Medicine, Jiading Branch of Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Shuang HeFudan University Shanghai Cancer Center, Institutes of Biomedical Sciences, New Cornerstone Science Laboratory, State Key Laboratory of Genetics and Development of Complex Phenotypes, Department of Biochemistry and Biophysics, School of Life Sciences, Shanghai Key Laboratory of Radiation Oncology and Shanghai Key Laboratory of Medical Epigenetics, Shanghai Medical College of Fudan University, Shanghai 200032, China.
Xizi ChenFudan University Shanghai Cancer Center, Institutes of Biomedical Sciences, New Cornerstone Science Laboratory, State Key Laboratory of Genetics and Development of Complex Phenotypes, Department of Biochemistry and Biophysics, School of Life Sciences, Shanghai Key Laboratory of Radiation Oncology and Shanghai Key Laboratory of Medical Epigenetics, Shanghai Medical College of Fudan University, Shanghai 200032, China.
Yanhui XuFudan University Shanghai Cancer Center, Institutes of Biomedical Sciences, New Cornerstone Science Laboratory, State Key Laboratory of Genetics and Development of Complex Phenotypes, Department of Biochemistry and Biophysics, School of Life Sciences, Shanghai Key Laboratory of Radiation Oncology and Shanghai Key Laboratory of Medical Epigenetics, Shanghai Medical College of Fudan University, Shanghai 200032, China.
Wenjuan WangReproduction Medical Center, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Yimin LaoDepartment of Biochemistry and Molecular Cell Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.
Bing LiDepartment of Biochemistry and Molecular Cell Biology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China.ORCID 0000-0002-7207-7117

Funding

China Postdoctoral Science Foundation 2025M772802CPSF GZC20251848Fundamental Research Funds for the Central UniversitiesNational Key R&D Program of China 2021YFA1300100National Natural Science Foundation of China 32030019National Natural Science Foundation of China 32500488National Natural Science Foundation of China 82072892Natural Science Foundation of Guangxi 2023GXNSFAA026276Natural Science Foundation of Shanghai 25ZR1402295Research Project of Jiading District Health Commission 2022-QN-02
6 · The paper itself

Abstract

Dysfunction of human chromatin remodeling complex switch/sucrose non-fermentable (hSWI/SNF) associates with multiple diseases including cancer. BCL7A, a tissue-specific, non-catalytic subunit of this complex, exhibits tumor--suppressive activity, especially in diffuse large B-cell lymphoma (DLBCL). However, the underlying mechanism remains elusive. In this study, we use protein structural prediction to identify a conserved arginine anchor in the N-terminal α-helix of BCL7A and demonstrate that this arginine anchor is crucial for the chromatin remodeling activity of the hSWI/SNF complexes. Truncation or DLBCL-associated mutations of this anchor impair BCL7A's tumor-suppressive function without affecting its integration into the complexes. Instead, these mutations lead to decreased BCL7A occupancy at target loci and reduced chromatin accessibility and transcriptional regulation. In vivo and cellular assays further validate the pivotal role of the arginine anchor in BCL7A-mediated tumor suppression. Mechanistically, we reveal that BCL7A regulates histone displacement, and its arginine anchor and the SMARCB1 subunit work cooperatively to regulate the remodeling activity of canonical BAF (BRG1/BRM-associated factor) complexes. Altogether, our study identifies the BCL7A arginine anchor as a key molecular switch that links nucleosome binding to chromatin remodeling and tumor suppression, making it a potential therapeutic target for DLBCL.

Indexed as

ArginineChromatin Assembly and DisassemblyLymphoma, Large B-Cell, DiffuseNucleosomesCell Line, TumorHumansSMARCB1 ProteinArginineNucleosomesSMARCB1 Proteinarginine anchorchromatin remodelingDLBCLhSWI/SNF

Identifiers

PMID41485079
PMCPMC13161475

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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.