ArticleNature communications2018
Mutant ASXL1 cooperates with BAP1 to promote myeloid leukaemogenesis.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
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Who cites it
89 citing papers in PubMed, 120 citations in OpenAlex.
- HMGB1 directly activates BAP1 transcription to sustain tumor growth in mesothelioma.Cell death and differentiation · 2026Article
- Condensates in fusion oncoprotein-driven leukemia: new biology and therapeutic opportunities.Trends in cancer · 2026Review
- Unique gluing effect of ASXL1 K351 monoubiquitination stimulates the PR-DUB activity.Nature chemical biology · 2026Article
- Modern Concepts in Precision Targeting of Acute Myeloid Leukemia Based on Principles of Molecular Oncology.Cancers · 2026Review
- TruncatingbioRxiv : the preprint server for biology · 2026Article
- BAP1 loss impairs IFN-γ signaling and enhances NK cell-mediated cytotoxicity in myeloid leukemia.Cancer immunology, immunotherapy : CII · 2026Article
- Prognostic impact of ASXL1 mutations in acute myeloid leukemia treated with lower intensity therapy.Cancer · 2026Article
- BAP1 and USP1 cooperate to regulate FANCD2 stability and cell proliferation in mesothelioma cells.Cell death & disease · 2026Article
- The Disordered Region of ASXL1 Acts as an Auto-Regulator Through Condensation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Unleashed condensation by recurrent mutations of an epigenetic regulator promotes cancer.bioRxiv : the preprint server for biology · 2026Article
- Recruitment of BRD4 to the ASXL1 genomic targets depends on the extra-terminal domain of BRD4.Nature communications · 2026Article
- Unconventional structure and function of PHD domains from additional sex combs-like proteins.The FEBS journal · 2025Article
- Analysis and Interpretation of Somatic NMD-Escaping Variants in Oncogenes and Dual-Function Genes across Adult and Pediatric Cancer Cohorts.medRxiv : the preprint server for health sciences · 2025Article
- The role of ASXL1, SRSF2, and EZH2 mutations in chromatin dysregulation of myelodysplastic neoplasia and acute myeloid leukemia.Leukemia · 2025Review
- Article
- ASXL1 mutation-related clonal hematopoiesis and age-related diseases: clinical evidence and molecular insights.International journal of hematology · 2025Review
- The Transgenerational Impact of High-Fat Diet and Diabetic Pregnancy on Embryonic Transcriptomics and Mitochondrial Health.Biomedicines · 2025Article
- UFMylation maintains tumor suppressor pVHL stability by activating the deubiquitinase BAP1.Science advances · 2025Article
- Epigenetic dysregulation in acute myeloid leukemia.Seminars in hematology · 2025Review
- Chronic myelomonocytic leukemia: molecular pathogenesis and therapeutic innovations.Haematologica · 2025Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
20 authors at 6 institutions in 3 countries.
Funding
Abstract
ASXL1 mutations occur frequently in myeloid neoplasms and are associated with poor prognosis. However, the mechanisms by which mutant ASXL1 induces leukaemogenesis remain unclear. In this study, we report mutually reinforcing effects between a C-terminally truncated form of mutant ASXL1 (ASXL1-MT) and BAP1 in promoting myeloid leukaemogenesis. BAP1 expression results in increased monoubiquitination of ASXL1-MT, which in turn increases the catalytic function of BAP1. This hyperactive ASXL1-MT/BAP1 complex promotes aberrant myeloid differentiation of haematopoietic progenitor cells and accelerates RUNX1-ETO-driven leukaemogenesis. Mechanistically, this complex induces upregulation of posterior HOXA genes and IRF8 through removal of H2AK119 ubiquitination. Importantly, BAP1 depletion inhibits posterior HOXA gene expression and leukaemogenicity of ASXL1-MT-expressing myeloid leukemia cells. Furthermore, BAP1 is also required for the growth of MLL-fusion leukemia cells with posterior HOXA gene dysregulation. These data indicate that BAP1, which has long been considered a tumor suppressor, in fact plays tumor-promoting roles in myeloid neoplasms.
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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.