Evidence map›Paper›PMID 28626217›Full record

ArticleLeukemia2018

Irf8 regulates the progression of myeloproliferative neoplasm-like syndrome via Mertk signaling in zebrafish.

F Zhao, Y Shi, Y Huang, Y Zhan, L Zhou, Y Li, Y Wan, H Li, H Huang, H Ruan and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Regulation of an lncRNAProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Zebrafish: a convenient tool for myelopoiesis research.Cell regeneration (London, England) · 2023
    Review
  8. Learning from Zebrafish Hematopoiesis.Advances in experimental medicine and biology · 2023
    Review
  9. Article
  10. Article
  11. Zebrafish models of acute leukemias: Current models and future directions.Wiley interdisciplinary reviews. Developmental biology · 2021
    Review
  12. Article
  13. Article
  14. Modeling hematopoietic disorders in zebrafish.Disease models & mechanisms · 2019
    Review
  15. Genetic Models of Leukemia in Zebrafish.Frontiers in cell and developmental biology · 2018
    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

12 authors at 2 institutions in 1 country.

F ZhaoKey Laboratory of Freshwater Fish Reproduction and Development, Ministry of Education, Key Laboratory of Aquatic Science of Chongqing, Laboratory of Molecular Developmental Biology, School of Life Sciences, Southwest University, Chongqing, China.
Y ShiKey Laboratory of Freshwater Fish Reproduction and Development, Ministry of Education, Key Laboratory of Aquatic Science of Chongqing, Laboratory of Molecular Developmental Biology, School of Life Sciences, Southwest University, Chongqing, China.
Y HuangKey Laboratory of Freshwater Fish Reproduction and Development, Ministry of Education, Key Laboratory of Aquatic Science of Chongqing, Laboratory of Molecular Developmental Biology, School of Life Sciences, Southwest University, Chongqing, China.
Y ZhanKey Laboratory of Freshwater Fish Reproduction and Development, Ministry of Education, Key Laboratory of Aquatic Science of Chongqing, Laboratory of Molecular Developmental Biology, School of Life Sciences, Southwest University, Chongqing, China.
L ZhouKey Laboratory of Freshwater Fish Reproduction and Development, Ministry of Education, Key Laboratory of Aquatic Science of Chongqing, Laboratory of Molecular Developmental Biology, School of Life Sciences, Southwest University, Chongqing, China.
Y LiBiomedical Analysis Center, Key Laboratory of Cytomics, The Third Military Medical University, Chongqing, China.
Y WanBiomedical Analysis Center, Key Laboratory of Cytomics, The Third Military Medical University, Chongqing, China.
H LiKey Laboratory of Freshwater Fish Reproduction and Development, Ministry of Education, Key Laboratory of Aquatic Science of Chongqing, Laboratory of Molecular Developmental Biology, School of Life Sciences, Southwest University, Chongqing, China.
H HuangKey Laboratory of Freshwater Fish Reproduction and Development, Ministry of Education, Key Laboratory of Aquatic Science of Chongqing, Laboratory of Molecular Developmental Biology, School of Life Sciences, Southwest University, Chongqing, China.
H RuanKey Laboratory of Freshwater Fish Reproduction and Development, Ministry of Education, Key Laboratory of Aquatic Science of Chongqing, Laboratory of Molecular Developmental Biology, School of Life Sciences, Southwest University, Chongqing, China.
L LuoKey Laboratory of Freshwater Fish Reproduction and Development, Ministry of Education, Key Laboratory of Aquatic Science of Chongqing, Laboratory of Molecular Developmental Biology, School of Life Sciences, Southwest University, Chongqing, China.
L LiKey Laboratory of Freshwater Fish Reproduction and Development, Ministry of Education, Key Laboratory of Aquatic Science of Chongqing, Laboratory of Molecular Developmental Biology, School of Life Sciences, Southwest University, Chongqing, China.
Southwest University · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interferon regulatory factor (IRF)-8 is a critical transcription factor involved in the pathogenesis of myeloid neoplasia. However, the underlying mechanisms in vivo are not well known. Investigation of irf8-mutant zebrafish in this study indicated that Irf8 is evolutionarily conserved as an essential neoplastic suppressor through tight control of the proliferation and longevity of myeloid cells. Surviving irf8 mutants quickly developed a myeloproliferative neoplasm (MPN)-like disease with enhanced output of the myeloid precursors, which recurred after transplantation. Multiple molecules presented notable alteration and Mertk signaling was aberrantly activated in the hematopoietic cells in irf8 mutants. Transgenic mertk overexpression in Tg(coro1a:mertk) zebrafish recapitulated the myeloid neoplasia-like syndrome in irf8 mutants. Moreover, functional interference with Mertk, via morpholino knockdown or genetic disruption, attenuated the myeloid expansion phenotype caused by Irf8 deficiency. Therefore, Mertk signaling is a critical downstream player in the Irf8-mediated regulation of the progression of myeloid neoplasia. Our study extends the understanding of the mechanisms underlying leukemogenesis.

Indexed as

AnimalsAnimals, Genetically ModifiedCell Proliferationc-Mer Tyrosine KinaseDisease ProgressionGene Expression RegulationInterferon Regulatory Factor-8Interferon Regulatory FactorsMyeloid CellsMyelopoiesisMyeloproliferative DisordersSignal TransductionZebrafishc-Mer Tyrosine KinaseInterferon Regulatory Factor-8Interferon Regulatory Factors

Identifiers

PMID28626217
OpenAlexW2660658786

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.