Evidence map›Paper›PMID 28416505›Full record

ReviewBlood2017

Hematopoietic transcription factor mutations: important players in inherited platelet defects.

Natthapol Songdej, A Koneti Rao

Open access · bronzeAbstract readReview
In one paragraph

Review in Blood, 2017. 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
5.6field-weighted citation impact, top 3% 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, 68 citations in OpenAlex.

  1. A novelHaematologica · 2026
    Article
  2. Characterization of a novelHaematologica · 2025
    Article
  3. Review
  4. Article
  5. Article
  6. Transcription factor RUNX1 regulates coagulation factor XIII-A (Research and practice in thrombosis and haemostasis · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. NovelCells · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Identification ofFrontiers in cell and developmental biology · 2021
    Article
  19. Article
  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

2 authors at 1 institution in 1 country.

Natthapol SongdejSol Sherry Thrombosis Research Center and Department of Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
A Koneti RaoSol Sherry Thrombosis Research Center and Department of Medicine, Lewis Katz School of Medicine at Temple University, Philadelphia, PA.ORCID 0000-0002-3078-7778
Temple University · US

Funding

Human Platelet Defects in Transcription Factor RUNX1 HaplodeficiencyR01HL109568 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI RAO, ANGARA KONETI · 2013 to 2022
$3.4M
NHLBI NIH HHS R01 HL109568
6 · The paper itself

Abstract

Transcription factors (TFs) are proteins that bind to specific DNA sequences and regulate expression of genes. The molecular and genetic mechanisms in most patients with inherited platelet defects are unknown. There is now increasing evidence that mutations in hematopoietic TFs are an important underlying cause for defects in platelet production, morphology, and function. The hematopoietic TFs implicated in patients with impaired platelet function and number include runt-related transcription factor 1, Fli-1 proto-oncogene, E-twenty-six (ETS) transcription factor (friend leukemia integration 1), GATA-binding protein 1, growth factor independent 1B transcriptional repressor, ETS variant 6, ecotropic viral integration site 1, and homeobox A11. These TFs act in a combinatorial manner to bind sequence-specific DNA within promoter regions to regulate lineage-specific gene expression, either as activators or repressors. TF mutations induce rippling downstream effects by simultaneously altering the expression of multiple genes. Mutations involving these TFs affect diverse aspects of megakaryocyte biology, and platelet production and function, culminating in thrombocytopenia and platelet dysfunction. Some are associated with predisposition to hematologic malignancies. These TF variants may occur more frequently in patients with inherited platelet defects than generally appreciated. This review focuses on alterations in hematopoietic TFs in the pathobiology of inherited platelet defects.

Indexed as

MutationBlood Platelet DisordersGenetic Diseases, InbornHematopoiesisHumansProto-Oncogene MasTranscription FactorsMAS1 protein, humanProto-Oncogene MasTranscription Factors

Identifiers

PMID28416505
PMCPMC5445569
OpenAlexW2605567733

What Socratic 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 Socratic graph.