ArticleCancer cell2018
A TFIID-SAGA Perturbation that Targets MYB and Suppresses Acute Myeloid Leukemia.
Article in Cancer cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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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.
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Who cites it
57 citing papers in PubMed, 75 citations in OpenAlex.
- Step-brothers in arms, SAGA and ATAC co-activator complexes, use different strategies.The EMBO journal · 2026Review
- PTBP1 controls oncogenic transcript processing and maintenance of acute myeloid leukemia.Leukemia · 2026Article
- An immunocompetent osteoblastic model of mammary cancer bone metastasis established by syngeneic intratibial injection of PyMT mammary carcinoma cells in FVB/N mice.bioRxiv : the preprint server for biology · 2026Article
- Disruption of the SAGA CORE triggers collateral degradation of KAT2A.Nature communications · 2026Article
- Article
- Regulation of NSL by TAF4A is critical for genome stability and quiescence of muscle stem cells.Nature communications · 2025Article
- Geminiviral replication enhancer hijacks a negative regulator of cytokinin signaling to facilitate viral infection.Plant communications · 2025Article
- The mechanism of YAP/TAZ transactivation and dual targeting for cancer therapy.Nature communications · 2025Article
- The lncRNA DUBR is regulated by CTCF and coordinates chromatin landscape and gene expression in hematopoietic cells.Nucleic acids research · 2025Article
- 3D chromatin hubs as regulatory units of identity and survival in human acute leukemia.Molecular cell · 2025Article
- The TATA-box binding protein-associated factor TAF12b facilitates the degradation of type B response regulators to negatively regulate cytokinin signaling.Plant communications · 2024Article
- Comparative cofactor screens show the influence of transactivation domains and core promoters on the mechanisms of transcription.Nature genetics · 2024Article
- TAF2, within the TFIID complex, regulates the expression of a subset of protein-coding genes.Cell death discovery · 2024Article
- Transcription Factor MYB as Therapeutic Target: Current Developments.International journal of molecular sciences · 2024Review
- Generation and optimization of off-the-shelf immunotherapeutics targeting TCR-Vβ2+ T cell malignancy.Nature communications · 2024Article
- MYB: A Key Transcription Factor in the Hematopoietic System Subject to Many Levels of Control.Advances in experimental medicine and biology · 2024Review
- MYB as a Critical Transcription Factor and Potential Therapeutic Target in AML.Advances in experimental medicine and biology · 2024Review
- Efficient genome editing in erythroid cells unveils novel MYB target genes and regulatory functions.iScience · 2023Article
- Synthetic oleanane triterpenoids suppressFrontiers in oncology · 2023Article
- Elevated TAF12 Expression Predicts Poor Prognosis in Glioma Patients: Evidence from Bioinformatic and Immunohistochemical Analyses.Biomolecules · 2022Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Targeting of general coactivators is an emerging strategy to interfere with oncogenic transcription factors (TFs). However, coactivator perturbations often lead to pleiotropic effects by influencing numerous TFs. Here we identify TAF12, a subunit of TFIID and SAGA coactivator complexes, as a selective requirement for acute myeloid leukemia (AML) progression. We trace this dependency to a direct interaction between the TAF12/TAF4 histone-fold heterodimer and the transactivation domain of MYB, a TF with established roles in leukemogenesis. Ectopic expression of the TAF4 histone-fold fragment can efficiently squelch TAF12 in cells, suppress MYB, and regress AML in mice. Our study reveals a strategy for potent MYB inhibition in AML and highlights how an oncogenic TF can be selectively neutralized by targeting a general coactivator complex.
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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.