Evidence map›Paper›PMID 25682601›Full record

ArticleHaematologica2015

Global transcriptome and chromatin occupancy analysis reveal the short isoform of GATA1 is deficient for erythroid specification and gene expression.

Timothy M Chlon, Maureen McNulty, Benjamin Goldenson, Alexander Rosinski, John D Crispino

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Over-Expressed GATA-1Antioxidants (Basel, Switzerland) · 2023
    Article
  6. Frontiers in genetics · 2023
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Acute Megakaryocytic Leukemia.Cold Spring Harbor perspectives in medicine · 2020
    Review
  19. Review
  20. Article
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 at 2 institutions in 1 country.

Timothy M ChlonDivision of Hematology/Oncology, Northwestern University, Chicago, IL, USA Present address Cincinnati Children's Hospital, Cincinnati, OH, USA.
Maureen McNultyDivision of Hematology/Oncology, Northwestern University, Chicago, IL, USA.
Benjamin GoldensonDivision of Hematology/Oncology, Northwestern University, Chicago, IL, USA.
Alexander RosinskiDivision of Hematology/Oncology, Northwestern University, Chicago, IL, USA.
John D CrispinoDivision of Hematology/Oncology, Northwestern University, Chicago, IL, USA j-crispino@northwestern.edu.
Northwestern University · USCincinnati Children's Hospital Medical Center · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LEONIDAS C. PLATANIAS · 1993 to 2026
$153.9M
CARCINOGENESIS TRAINING PROGRAMT32CA009560 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Kathleen Janee Green · 1986 to 2026
$8.4M
Training Program in Cancer TherapeuticsT32CA117846 · NCI · UNIVERSITY OF CINCINNATI · PI PRICE, CAROLYN M, TAKIAR, VINITA · 2006 to 2022
$6.5M
GATA1 Mutation in Defective ErythropoiesisR01DK101329 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CRISPINO, JOHN D · 2013 to 2017
$1.7M
NCI NIH HHS P30 CA060553NCI NIH HHS T32 CA009560NCI NIH HHS T32 CA117846NIDDK NIH HHS DK101329NIDDK NIH HHS R01 DK101329
6 · The paper itself

Abstract

GATA1 is a master transcriptional regulator of the differentiation of several related myeloid blood cell types, including erythrocytes and megakaryocytes. Germ-line mutations that cause loss of full length GATA1, but allow for expression of the short isoform (GATA1s), are associated with defective erythropoiesis in a subset of patients with Diamond Blackfan Anemia. Despite extensive studies of GATA1s in megakaryopoiesis, the mechanism by which GATA1s fails to support normal erythropoiesis is not understood. In this study, we used global gene expression and chromatin occupancy analysis to compare the transcriptional activity of GATA1s to GATA1. We discovered that compared to GATA1, GATA1s is less able to activate the erythroid gene expression program and terminal differentiation in cells with dual erythroid-megakaryocytic differentiation potential. Moreover, we found that GATA1s bound to many of its erythroid-specific target genes less efficiently than full length GATA1. These results suggest that the impaired ability of GATA1s to promote erythropoiesis in DBA may be caused by failure to occupy erythroid-specific gene regulatory elements.

Indexed as

Chromatin ImmunoprecipitationGene Expression RegulationRNA IsoformsTranscriptomeBinding SitesCell DifferentiationCell LineCluster AnalysisErythroid CellsErythropoiesisGATA1 Transcription FactorGene Expression ProfilingHumansMegakaryocytesNucleotide MotifsProtein BindingGATA1 Transcription FactorRNA Isoforms

Identifiers

PMID25682601
PMCPMC4420206
OpenAlexW2118518129

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.