ArticleNucleic acids research2011
Tumour suppressor ING1b maintains genomic stability upon replication stress.
Article in Nucleic acids research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- The INO80 chromatin remodeller facilitates DNA damage bypass via postreplicative gap repair.The EMBO journal · 2025Article
- RAD18 methylation by the methyltransferase SETD6 attenuates DNA breaks.Scientific reports · 2025Article
- ING2 Controls Mitochondrial RespirationFrontiers in cell and developmental biology · 2021Article
- Focus-ING on DNA Integrity: Implication of ING Proteins in Cell Cycle Regulation and DNA Repair Modulation.Cancers · 2019Review
- ING3 is required for ATM signaling and DNA repair in response to DNA double strand breaks.Cell death and differentiation · 2019Article
- ING1b negatively regulates HIF1α protein levels in adipose-derived stromal cells by a SUMOylation-dependent mechanism.Cell death & disease · 2015Article
- SUMOylation of the ING1b tumor suppressor regulates gene transcription.Carcinogenesis · 2014Article
- ING4 regulates a secretory phenotype in primary fibroblasts with dual effects on cell proliferation and tumor growth.Oncogene · 2014Article
- ING1 and ING2: multifaceted tumor suppressor genes.Cellular and molecular life sciences : CMLS · 2013Review
- ING1 induces apoptosis through direct effects at the mitochondria.Cell death & disease · 2013Article
- Inhibitor of growth 1 (ING1) acts at early steps of multiple DNA repair pathways.Molecular and cellular biochemistry · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The lesion bypass pathway, which is regulated by monoubiquitination of proliferating cell nuclear antigen (PCNA), is essential for resolving replication stalling due to DNA lesions. This process is important for preventing genomic instability and cancer development. Previously, it was shown that cells deficient in tumour suppressor p33ING1 (ING1b) are hypersensitive to DNA damaging agents via unknown mechanism. In this study, we demonstrated a novel tumour suppressive function of ING1b in preserving genomic stability upon replication stress through regulating PCNA monoubiquitination. We found that ING1b knockdown cells are more sensitive to UV due to defects in recovering from UV-induced replication blockage, leading to enhanced genomic instability. We revealed that ING1b is required for the E3 ligase Rad18-mediated PCNA monoubiquitination in lesion bypass. Interestingly, ING1b-mediated PCNA monoubiquitination is associated with the regulation of histone H4 acetylation. Results indicate that chromatin remodelling contributes to the stabilization of stalled replication fork and to the regulation of PCNA monoubiquitination during lesion bypass.
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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.