Evidence map›Paper›PMID 26010396›Full record

ArticleBritish journal of haematology2015

Loss of RUNX1/AML1 arginine-methylation impairs peripheral T cell homeostasis.

Shinsuke Mizutani, Tatsushi Yoshida, Xinyang Zhao, Stephen D Nimer, Masafumi Taniwaki, Tsukasa Okuda

Open access · bronzeAbstract read
In one paragraph

Article in British journal of haematology, 2015. 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
0.6field-weighted citation impact, top 31% 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, 22 citations in OpenAlex.

  1. Article
  2. Lysine and arginine methylation of transcription factors.Cellular and molecular life sciences : CMLS · 2024
    Review
  3. Transcriptional network dynamics in early T cell development.The Journal of experimental medicine · 2024
    Review
  4. Review
  5. Review
  6. Protein arginine methylation in transcription and epigenetic regulation.Frontiers in epigenetics and epigenomics · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. 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

6 authors at 3 institutions in 2 countries.

Shinsuke MizutaniDepartment of Biochemistry and Molecular Biology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan.
Tatsushi YoshidaDepartment of Biochemistry and Molecular Biology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan.
Xinyang ZhaoDepartment of Biochemistry & Molecular Genetics, University of Alabama, Birmingham, AL, USA.
Stephen D NimerSylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, Miami, FL, USA.
Masafumi TaniwakiDivision of Haematology and Oncology, Department of Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Tsukasa OkudaDepartment of Biochemistry and Molecular Biology, Kyoto Prefectural University of Medicine Graduate School of Medical Science, Kyoto, Japan.
Kyoto Prefectural University of Medicine · JPUniversity of Alabama at Birmingham · USUniversity of Miami · US

Funding

Targeting p300 and lysine acetylation in AMLR01CA166835 · NCI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Stephen D. Nimer · 2012 to 2026
$4.6M
NCI NIH HHS R01 CA166835
6 · The paper itself

Abstract

RUNX1 (previously termed AML1) is a frequent target of human leukaemia-associated gene aberrations, and it encodes the DNA-binding subunit of the Core-Binding Factor transcription factor complex. RUNX1 expression is essential for the initiation of definitive haematopoiesis, for steady-state thrombopoiesis, and for normal lymphocytes development. Recent studies revealed that protein arginine methyltransferase 1 (PRMT1), which accounts for the majority of the type I PRMT activity in cells, methylates two arginine residues in RUNX1 (R206 and R210), and these modifications inhibit corepressor-binding to RUNX1 thereby enhancing its transcriptional activity. In order to elucidate the biological significance of these methylations, we established novel knock-in mouse lines with non-methylable, double arginine-to-lysine (RTAMR-to-KTAMK) mutations in RUNX1. Homozygous Runx1(KTAMK) (/) (KTAMK) mice are born alive and appear normal during adulthood. However, Runx1(KTAMK) (/) (KTAMK) mice showed a reduction in CD3(+) T lymphoid cells and a decrease in CD4(+) T cells in peripheral lymphoid organs, in comparison to their wild-type littermates, leading to a reduction in the CD4(+) to CD8(+) T-cell ratio. These findings suggest that arginine-methylation of RUNX1 in the RTAMR-motif is dispensable for the development of definitive haematopoiesis and for steady-state platelet production, however this modification affects the role of RUNX1 in the maintenance of the peripheral CD4(+) T-cell population.

Indexed as

HematopoiesisAllelesAmino Acid MotifsAnimalsArginineCD4 Lymphocyte CountCore Binding Factor Alpha 2 SubunitEmbryonic Stem CellsGene Knock-In TechniquesGene OrderGene TargetingGenetic VectorsGenotypeGerm CellsHumansMethylationArginineCore Binding Factor Alpha 2 Subunitleukaemialymphocyte differentiationmethylationRUNX1transgenic mice models

Identifiers

PMID26010396
PMCPMC4996932
OpenAlexW1947842590

What OpenQuestion holds

Textmetadata
LicenceTDM
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.