ArticleNucleic acids research2017
A c-Myb mutant causes deregulated differentiation due to impaired histone binding and abrogated pioneer factor function.
Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Bibliometric Analysis of ATAC-Seq and Its Use in Cancer Biology via Nucleic Acid Detection.Frontiers in medicine · 2020Pooled it
- Insights from pooled CRISPRi single-cell screens in K562 cells reveal gene functions, regulatory networks, and highlight opportunities and limitations.BMC genomics · 2026Article
- Transcriptional regulatory program controlled by MYB in T-cell acute lymphoblastic leukemia.Leukemia · 2024Article
- The ETO2 transcriptional cofactor maintains acute leukemia by driving a MYB/EP300-dependent stemness program.HemaSphere · 2024Article
- MYB: A Key Transcription Factor in the Hematopoietic System Subject to Many Levels of Control.Advances in experimental medicine and biology · 2024Review
- Molecular dynamics simulation reveals DNA-specific recognition mechanism via c-Myb in pseudo-palindromic consensus ofJournal of Zhejiang University. Science. B · 2023Article
- MYB insufficiency disrupts proteostasis in hematopoietic stem cells, leading to age-related neoplasia.Blood · 2023Article
- Synthetic oleanane triterpenoids suppressFrontiers in oncology · 2023Article
- c-Myb Dominates TBK1-Mediated Endotoxin Tolerance in Kupffer Cells by Negatively Regulating DTX4.Journal of immunology research · 2023Article
- Article
- SOX9 reprograms endothelial cells by altering the chromatin landscape.Nucleic acids research · 2022Article
- Pioneer transcription factors are associated with the modulation of DNA methylation patterns across cancers.Epigenetics & chromatin · 2022Article
- Chromatin occupancy and target genes of the haematopoietic master transcription factor MYB.Scientific reports · 2021Article
- Regulation of MYB by distal enhancer elements in human myeloid leukemia.Cell death & disease · 2021Article
- Dissecting the transactivation domain (tAD) of the transcription factor c-Myb to assess recent models of tAD function.FEBS open bio · 2020Article
- c-Myb regulates tumorigenic potential of embryonal rhabdomyosarcoma cells.Scientific reports · 2019Article
- The EZH2 SANT1 domain is a histone reader providing sensitivity to the modification state of the H4 tail.Scientific reports · 2019Article
- Reading More than Histones: The Prevalence of Nucleic Acid Binding among Reader Domains.Molecules (Basel, Switzerland) · 2018Review
- The SUMO protease SENP1 and the chromatin remodeler CHD3 interact and jointly affect chromatin accessibility and gene expression.The Journal of biological chemistry · 2018Article
- The pioneer factor activity of c-Myb involves recruitment of p300 and induction of histone acetylation followed by acetylation-induced chromatin dissociation.Epigenetics & chromatin · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor c-Myb is involved in early differentiation and proliferation of haematopoietic cells, where it operates as a regulator of self-renewal and multi-lineage differentiation. Deregulated c-Myb plays critical roles in leukaemias and other human cancers. Due to its role as a master regulator, we hypothesized it might function as a pioneer transcription factor. Our approach to test this was to analyse a mutant of c-Myb, D152V, previously reported to cause haematopoietic defects in mice by an unknown mechanism. Our transcriptome data from K562 cells indicates that this mutation specifically affects c-Myb's ability to regulate genes involved in differentiation, causing failure in c-Myb's ability to block differentiation. Furthermore, we see a major effect of this mutation in assays where chromatin opening is involved. We show that each repeat in the minimal DNA-binding domain of c-Myb binds to histones and that D152V disrupts histone binding of the third repeat. ATAC-seq data indicates this mutation impairs the ability of c-Myb to cause chromatin opening at specific sites. Taken together, our findings support that c-Myb acts as a pioneer factor and show that D152V impairs this function. The D152V mutant is the first mutant of a transcription factor specifically destroying pioneer factor function.
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.