Evidence map›Paper›PMID 15860665›Full record

ArticleBlood2005

Differential requirements for the activation domain and FOG-interaction surface of GATA-1 in megakaryocyte gene expression and development.

Andrew G Muntean, John D Crispino

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

72 citing papers in PubMed, 122 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. GATA1 in Normal and Pathologic Megakaryopoiesis and Platelet Development.Advances in experimental medicine and biology · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Acute Megakaryocytic Leukemia.Cold Spring Harbor perspectives in medicine · 2020
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Haematologica · 2017
    Article
  19. Review
  20. Article

12 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Andrew G MunteanBen May Institute for Cancer Research, Univeristy of Chicago, IL, USA.
John D Crispino
University of Chicago · US

Funding

Mechanisms of Leukemogenesis in Down SyndromeR01CA101774 · NCI · UNIVERSITY OF CHICAGO · PI CRISPINO, JOHN D · 2003 to 2021
$6.1M
NCI NIH HHS R01 CA-101774NCI NIH HHS R01 CA101774
6 · The paper itself

Abstract

GATA1 is mutated in patients with 2 different disorders. First, individuals with a GATA1 mutation that blocks the interaction between GATA-1 and its cofactor Friend of GATA-1 (FOG-1) suffer from dyserythropoietic anemia and thrombocytopenia. Second, children with Down syndrome who develop acute megakaryoblastic leukemia harbor mutations in GATA1 that lead to the exclusive expression of a shorter isoform named GATA-1s. To determine the effect of these patient-specific mutations on GATA-1 function, we first compared the gene expression profile between wild-type and GATA-1-deficient megakaryocytes. Next, we introduced either GATA-1s or a FOG-binding mutant (V205G) into GATA-1-deficient megakaryocytes and assessed the effect on differentiation and gene expression. Whereas GATA-1-deficient megakaryocytes failed to undergo terminal differentiation and proliferated excessively in vitro, GATA-1s-expressing cells displayed proplatelet formation and other features of terminal maturation, but continued to proliferate aberrantly. In contrast, megakaryocytes that expressed V205G GATA-1 exhibited reduced proliferation, but failed to undergo maturation. Examination of the expression of megakaryocyte-specific genes in the various rescued cells correlated with the observed phenotypic differences. These studies show that GATA-1 is required for both normal regulation of proliferation and terminal maturation of megakaryocytes, and further, that these functions can be uncoupled by mutations in GATA1.

Indexed as

Anemia, Dyserythropoietic, CongenitalAnimalsBinding SitesCarrier ProteinsCell DifferentiationCell ProliferationDNA-Binding ProteinsDown SyndromeErythroid-Specific DNA-Binding FactorsGATA1 Transcription FactorGene Expression ProfilingGene Expression RegulationMegakaryocytesMiceMice, Inbred C57BLMutationCarrier ProteinsDNA-Binding ProteinsErythroid-Specific DNA-Binding FactorsGata1 protein, mouseGATA1 Transcription FactorNuclear ProteinsTranscription FactorsZfpm1 protein, mouse

Identifiers

PMID15860665
PMCPMC1895209
OpenAlexW2046286855

What OpenQuestion holds

Textmetadata
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.