Evidence map›Paper›PMID 26382271›Full record

ArticlePloS one2015

Regulation of the Flt3 Gene in Haematopoietic Stem and Early Progenitor Cells.

Giacomo Volpe, Mary Clarke, Paloma Garcìa, David Scott Walton, Alexandros Vegiopoulos, Walter Del Pozzo, Laura Patricia O'Neill, Jonathan Frampton, Stéphanie Dumon

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
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

18 citing papers in PubMed, 25 citations in OpenAlex.

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  12. Modeling the Hematopoietic Landscape.Frontiers in cell and developmental biology · 2019
    Review
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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

9 authors at 2 institutions in 2 countries.

Giacomo VolpeInstitute of Biomedical Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, B15 2TT, United Kingdom.
Mary ClarkeInstitute of Biomedical Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, B15 2TT, United Kingdom.
Paloma GarcìaInstitute of Biomedical Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, B15 2TT, United Kingdom.
David Scott WaltonInstitute of Biomedical Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, B15 2TT, United Kingdom.
Alexandros VegiopoulosDKFZ Junior Group Metabolism and Stem Cell Plasticity, Division of Molecular Metabolic Control (A170), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Walter Del PozzoSchool of Physics and Astronomy, University of Birmingham, Birmingham, B15 2TT, United Kingdom.
Laura Patricia O'NeillInstitute of Biomedical Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, B15 2TT, United Kingdom.
Jonathan FramptonInstitute of Biomedical Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, B15 2TT, United Kingdom.
Stéphanie DumonInstitute of Biomedical Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, B15 2TT, United Kingdom.
University of Birmingham · GBHeidelberg University · DE

Funding

Medical Research Council G0501688Medical Research Council MR/K01076X/1
6 · The paper itself

Abstract

The MYB transcription factor plays critical roles in normal and malignant haematopoiesis. We previously showed that MYB was a direct activator of FLT3 expression within the context of acute myeloid leukaemia. During normal haematopoiesis, increasing levels of FLT3 expression determine a strict hierarchy within the haematopoietic stem and early progenitor compartment, which associates with lymphoid and myeloid commitment potential. We use the conditional deletion of the Myb gene to investigate the influence of MYB in Flt3 transcriptional regulation within the haematopoietic stem cell (HSC) hierarchy. In accordance with previous report, in vivo deletion of Myb resulted in rapid biased differentiation of HSC with concomitant loss of proliferation capacity. We find that loss of MYB activity also coincided with decreased FLT3 expression. At the chromatin level, the Flt3 promoter is primed in immature HSC, but occupancy of further intronic elements determines expression. Binding to these locations, MYB and C/EBPα need functional cooperation to activate transcription of the locus. This cooperation is cell context dependent and indicates that MYB and C/EBPα activities are inter-dependent in controlling Flt3 expression to influence lineage commitment of multipotential progenitors.

Indexed as

AnimalsCCAAT-Enhancer-Binding ProteinsCell DifferentiationCell LineageCells, Culturedfms-Like Tyrosine Kinase 3Gene Expression RegulationHematopoiesisHematopoietic Stem CellsMiceMice, Inbred C57BLMice, TransgenicOncogene Proteins v-mybCCAAT-Enhancer-Binding ProteinsCEBPA protein, mouseFlt3 protein, mousefms-Like Tyrosine Kinase 3Oncogene Proteins v-myb

Identifiers

PMID26382271
PMCPMC4575200
OpenAlexW2337995955

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.