ArticleProceedings of the National Academy of Sciences of the United States of America2010
L3MBTL1 polycomb protein, a candidate tumor suppressor in del(20q12) myeloid disorders, is essential for genome stability.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 87 citations in OpenAlex.
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- Nucleosome context regulates chromatin reader preference.Nucleic acids research · 2025Article
- Nutrigenomic insights and cardiovascular benefits of blackberry (Rubus ulmifolius Schott.) and mugwort (Artemisia campestris L.).Experimental physiology · 2025Article
- Prognostic impact of somatic mutations and additional chromosomal abnormalities in patients with myelodysplastic syndromes and chromosome 20q deletion.Clinical and experimental medicine · 2025Article
- Chronic Wound Initiation: Single-Cell RNAseq of Cutaneous Wound Tissue and Contributions of Oxidative Stress to Initiation of Chronicity.Antioxidants (Basel, Switzerland) · 2025Article
- L3MBTL1, a polycomb protein, promotes Osimertinib acquired resistance through epigenetic regulation of DNA damage response in lung adenocarcinoma.Cell death & disease · 2024Article
- Altered methylation of imprinted genes in neuroblastoma: implications for prognostic refinement.Journal of translational medicine · 2024Article
- Construction and validation of a chromatin regulator-related gene signature for prognostic and therapeutic significance of clear cell renal cell carcinoma.Translational cancer research · 2024Article
- Sticky, Adaptable, and Many-sided: SAM protein versatility in normal and pathological hematopoietic states.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023Review
- Effect of L3MBTL3/PTPN9 polymorphisms on risk to alcohol-induced ONFH in Chinese Han population.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Article
- An Integrative Systems Biology Approach Identifies Molecular Signatures Associated with Gallbladder Cancer Pathogenesis.Journal of clinical medicine · 2021Article
- Targeting epigenetic protein-protein interactions with small-molecule inhibitors.Future medicinal chemistry · 2020Review
- MYCN is amplified during S phase, and c‑myb is involved in controlling MYCN expression and amplification in MYCN‑amplified neuroblastoma cell lines.Molecular medicine reports · 2019Article
- Activity-Induced Regulation of Synaptic Strength through the Chromatin Reader L3mbtl1.Cell reports · 2018Article
- L3MBTL2 orchestrates ubiquitin signalling by dictating the sequential recruitment of RNF8 and RNF168 after DNA damage.Nature cell biology · 2018Article
- Aging and the rise of somatic cancer-associated mutations in normal tissues.PLoS genetics · 2018Review
- Spatially restricted loading of BRD2 at DNA double-strand breaks protects H4 acetylation domains and promotes DNA repair.Scientific reports · 2017Article
- The tale of a tail: histone H4 acetylation and the repair of DNA breaks.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The l3mbtl1 gene is located on the long arm of chromosome 20 (q12), within a region commonly deleted in several myeloid malignancies. L3MBTL1 is a human homolog of the Drosophila polycomb L(3)MBT tumor suppressor protein and thus a candidate tumor suppressor in del(20q12) myeloid disorders. We used the loss-of-function approach to explore the possible tumor suppressive mechanism of L3MBTL1 and found that depletion of L3MBTL1 from human cells causes replicative stress, DNA breaks, activation of the DNA damage response, and genomic instability. L3MBTL1 interacts with Cdc45, MCM2-7 and PCNA, components of the DNA replication machinery, and is required for normal replication fork progression, suggesting that L3MBTL1 causes DNA damage, at least in part, by perturbing DNA replication. An activated DNA damage response and genomic instability are common features in tumorigenesis and a consequence of overexpression of many oncogenes. We propose that the loss of L3MBTL1 contributes to the development of 20q(-) hematopoietic malignancies by inducing replicative stress, DNA damage, and genomic instability.
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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.