Evidence map›Paper›PMID 16195416›Full record

ArticleGenes & development2005

Histone H3 tail positioning and acetylation by the c-Myb but not the v-Myb DNA-binding SANT domain.

Xianming Mo, Elisabeth Kowenz-Leutz, Yves Laumonnier, Hong Xu, Achim Leutz

Abstract read
In one paragraph

Article in Genes & development, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed.

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  18. Article
  19. Review
  20. Myb proteins: angels and demons in normal and transformed cells.Frontiers in bioscience (Landmark edition) · 2011
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Xianming MoMax-Delbrueck-Center for Molecular Medicine, 13092 Berlin, Germany.
Elisabeth Kowenz-Leutz
Yves Laumonnier
Hong Xu
Achim Leutz

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The c-Myb transcription factor coordinates proliferation and differentiation of hematopoietic precursor cells. Myb has three consecutive N-terminal SANT-type repeat domains (R1, R2, R3), two of which (R2, R3) form the DNA-binding domain (DBD). Three amino acid substitutions in R2 alter the way Myb regulates genes and determine the leukemogenicity of the retrovirally transduced v-Myb oncogene. The molecular mechanism of how these mutations unleash the leukemogenic potential of Myb is unknown. Here we demonstrate that the c-Myb-DBD binds to the N-terminal histone tails of H3 and H3.3. C-Myb binding facilitates histone tail acetylation, which is mandatory during activation of prevalent differentiation genes in conjunction with CCAAT enhancer-binding proteins (C/EBP). Leukemogenic mutations in v-Myb eliminate the interaction with H3 and acetylation of H3 tails and abolish activation of endogenous differentiation genes. In primary v-myb-transformed myeloblasts, pharmacologic enhancement of H3 acetylation restored activation of differentiation genes and induced cell differentiation. Our data link a novel chromatin function of c-Myb with lineage-specific expression of differentiation genes and relate the loss of this function with the leukemic conversion of Myb.

Indexed as

AcetylationAmino Acid SubstitutionAnimalsBase SequenceCCAAT-Binding FactorCell DifferentiationCells, CulturedChickensChromatinGene Expression RegulationGene Expression Regulation, LeukemicGranulocyte Precursor CellsHistonesHumansLeukemiaMolecular Sequence DataCCAAT-Binding FactorChromatinHistonesOncogene Proteins v-mybProto-Oncogene Proteins c-myb

Identifiers

PMID16195416
PMCPMC1257399

What OpenQuestion holds

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Registered trials

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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.