ArticleThe Journal of cell biology2020
Loss of CBX2 induces genome instability and senescence-associated chromosomal rearrangements.
Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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.
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.
Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- CBX2 phase-separation contributes to homologous recombination repair and drug resistance in ovarian cancer.Cell death & disease · 2026Article
- Construction and validation of gene signature for prognosis and drug sensitivity in cholangiocarcinoma based on cellular senescence related genes.Scientific reports · 2025Article
- Interrogating the regulatory epigenome of cellular senescence.Cellular and molecular life sciences : CMLS · 2025Review
- Construction and validation of a cell-in-cell related prognostic signature for hepatocellular carcinoma.Discover oncology · 2025Article
- Single-cell and bulk transcriptional profiling of mouse ovaries reveals novel genes and pathways associated with DNA damage response in oocytes.Developmental biology · 2025Article
- Uncovering the role of aquaporin and chromobox family members as potential biomarkers in head and neck squamous cell carcinoma via integrative multiomics and in silico approach.Journal of applied genetics · 2024Article
- Single-cell and bulk transcriptional profiling of mouse ovaries reveals novel genes and pathways associated with DNA damage response in oocytes.bioRxiv : the preprint server for biology · 2024Article
- Acute irradiation induces a senescence-like chromatin structure in mammalian oocytes.Communications biology · 2023Article
- Indicators of HSV1 Infection, ECM-Receptor Interaction, and Chromatin Modulation in a Nuclear Family with Schizophrenia.Journal of personalized medicine · 2023Article
- Proteomic profiling across breast cancer cell lines and models.Scientific data · 2023Article
- Computational screen to identify potential targets for immunotherapeutic identification and removal of senescence cells.Aging cell · 2023Article
- Down-regulation of Jun induces senescence through destabilizing chromatin in osteoarthritis chondrocytes.American journal of translational research · 2023Article
- Comprehensive Analysis of Cellular Senescence-Related Genes in Prognosis, Molecular Characterization and Immunotherapy of Hepatocellular Carcinoma.Biological procedures online · 2022Article
- PAHSAs reduce cellular senescence and protect pancreatic beta cells from metabolic stress through regulation of Mdm2/p53.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- CBX4 Regulates Replicative Senescence of WI-38 Fibroblasts.Oxidative medicine and cellular longevity · 2022Article
- Loss of polycomb repressive complex 1 activity and chromosomal instability drive uveal melanoma progression.Nature communications · 2021Article
- Single-molecule imaging of epigenetic complexes in living cells: insights from studies on Polycomb group proteins.Nucleic acids research · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The polycomb group protein CBX2 is an important epigenetic reader involved in cell proliferation and differentiation. While CBX2 overexpression occurs in a wide range of human tumors, targeted deletion results in homeotic transformation, proliferative defects, and premature senescence. However, its cellular function(s) and whether it plays a role in maintenance of genome stability remain to be determined. Here, we demonstrate that loss of CBX2 in mouse fibroblasts induces abnormal large-scale chromatin structure and chromosome instability. Integrative transcriptome analysis and ATAC-seq revealed a significant dysregulation of transcripts involved in DNA repair, chromocenter formation, and tumorigenesis in addition to changes in chromatin accessibility of genes involved in lateral sclerosis, basal transcription factors, and folate metabolism. Notably, Cbx2-/- cells exhibit prominent decondensation of satellite DNA sequences at metaphase and increased sister chromatid recombination events leading to rampant chromosome instability. The presence of extensive centromere and telomere defects suggests a prominent role for CBX2 in heterochromatin homeostasis and the regulation of nuclear architecture.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.