Evidence map›Paper›PMID 37149540›Full record

ArticleInternational journal of hematology2023

EBF1-JAK2 inhibits the PAX5 function through physical interaction with PAX5 and kinase activity.

Yukino Kojima, Fumika Kawashima, Takahiko Yasuda, Koya Odaira, Yuichiro Inagaki, Chiharu Yamada, Ami Muraki, Mina Noura, Shuichi Okamoto, Shogo Tamura and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in International journal of hematology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

18 authors at 7 institutions in 1 country.

Yukino Kojima *Division of Cellular and Genetic Sciences, Department of Integrated Health Sciences, Nagoya University Graduate School of Medicine, 1-1-20 Daiko-Minami, Higashi-ku, Nagoya, 461-0047, Japan.
Fumika Kawashima *Division of Cellular and Genetic Sciences, Department of Integrated Health Sciences, Nagoya University Graduate School of Medicine, 1-1-20 Daiko-Minami, Higashi-ku, Nagoya, 461-0047, Japan.
Takahiko YasudaClinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan.
Koya OdairaDivision of Cellular and Genetic Sciences, Department of Integrated Health Sciences, Nagoya University Graduate School of Medicine, 1-1-20 Daiko-Minami, Higashi-ku, Nagoya, 461-0047, Japan.
Yuichiro InagakiDepartment of Hematology and Oncology, Anjo Kosei Hospital, Anjo, Japan.
Chiharu YamadaDivision of Cellular and Genetic Sciences, Department of Integrated Health Sciences, Nagoya University Graduate School of Medicine, 1-1-20 Daiko-Minami, Higashi-ku, Nagoya, 461-0047, Japan.
Ami MurakiDivision of Cellular and Genetic Sciences, Department of Integrated Health Sciences, Nagoya University Graduate School of Medicine, 1-1-20 Daiko-Minami, Higashi-ku, Nagoya, 461-0047, Japan.
Mina NouraDivision of Cellular and Genetic Sciences, Department of Integrated Health Sciences, Nagoya University Graduate School of Medicine, 1-1-20 Daiko-Minami, Higashi-ku, Nagoya, 461-0047, Japan.
Shuichi OkamotoDivision of Cellular and Genetic Sciences, Department of Integrated Health Sciences, Nagoya University Graduate School of Medicine, 1-1-20 Daiko-Minami, Higashi-ku, Nagoya, 461-0047, Japan.
Shogo TamuraDivision of Cellular and Genetic Sciences, Department of Integrated Health Sciences, Nagoya University Graduate School of Medicine, 1-1-20 Daiko-Minami, Higashi-ku, Nagoya, 461-0047, Japan.
Eisuke IwamotoClinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan.
Masashi SanadaClinical Research Center, National Hospital Organization Nagoya Medical Center, Nagoya, Japan.
Itaru MatsumuraDepartment of Hematology and Rheumatology, Kindai University School of Medicine, Osaka, Japan.
Yasushi MiyazakiDepartment of Hematology, Atomic Bomb Disease and Hibakusha Medicine Unit, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan.
Tetsuhito KojimaDivision of Cellular and Genetic Sciences, Department of Integrated Health Sciences, Nagoya University Graduate School of Medicine, 1-1-20 Daiko-Minami, Higashi-ku, Nagoya, 461-0047, Japan.
Hitoshi KiyoiDepartment of Hematology and Oncology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Shinobu TsuzukiDepartment of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Japan.
Fumihiko HayakawaDivision of Cellular and Genetic Sciences, Department of Integrated Health Sciences, Nagoya University Graduate School of Medicine, 1-1-20 Daiko-Minami, Higashi-ku, Nagoya, 461-0047, Japan. bun-hy@med.nagoya-u.ac.jp.ORCID http://orcid.org/0000-0002-6067-6382
Nagoya University · JPNational Hospital Organization · JPAichi Health Promotion Foundation · JPAichi Medical University · JPAnjo Kosei Hospital · JPKindai University · JPNagasaki University · JP

Funding

Japan Agency for Medical Research and Development JP16ck0106129Japan Agency for Medical Research and Development JP19ck0106331Japan Agency for Medical Research and Development JP22ck0106607Japan Society for the Promotion of Science 18H02835Japan Society for the Promotion of Science 21K19505Japan Society for the Promotion of Science 22H03102
6 · The paper itself

Abstract

Gene aberrations of B-cell regulators and growth signal components such as the JAK-STAT pathway are frequently found in B-cell acute lymphoblastic leukemia (B-ALL). EBF1 is a B-cell regulator that regulates the expression of PAX5 and co-operates with PAX5 to regulate B-cell differentiation. Here, we analyzed the function of the fusion protein of EBF1 and JAK2, EBF1-JAK2 (E-J). E-J caused constitutive activation of JAK-STAT and MAPK pathways and induced autonomous cell growth in a cytokine-dependent cell line. E-J did not affect the transcriptional activity of EBF1 but inhibited that of PAX5. Both the physical interaction of E-J with PAX5 and kinase activity of E-J were required for E-J to inhibit PAX5 function, although the detailed mechanism of inhibition remains unclear. Importantly, gene set enrichment analysis using the results of our previous RNA-seq data of 323 primary BCR-ABL1-negative ALL samples demonstrated repression of the transcriptional target genes of PAX5 in E-J-positive ALL cells, which suggests that E-J also inhibited PAX5 function in ALL cells. Our results shed new light on the mechanisms of differentiation block by kinase fusion proteins.

Indexed as

Janus KinasesSTAT Transcription FactorsCell LineHumansJanus Kinase 2PAX5 Transcription FactorSignal TransductionTrans-ActivatorsTranscription FactorsEBF1 protein, humanJAK2 protein, humanJanus Kinase 2Janus KinasesPAX5 protein, humanPAX5 Transcription FactorSTAT Transcription FactorsTrans-ActivatorsTranscription FactorsAcute lymphoblastic leukemiaEBF1–JAK2PAX5PhosphorylationRNA-seq

Identifiers

PMID37149540
OpenAlexW4372310828

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.