Evidence map›Paper›PMID 37922454›Full record

ArticleBlood2024

Regulation of lymphoid-myeloid lineage bias through regnase-1/3-mediated control of Nfkbiz.

Takuya Uehata, Shinnosuke Yamada, Daisuke Ori, Alexis Vandenbon, Amir Giladi, Adam Jelinski, Yasuhiro Murakawa, Hitomi Watanabe, Kazuhiro Takeuchi, Kazunori Toratani and 13 more

Open access · hybridAbstract read
In one paragraph

Article in Blood, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

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  6. Regulation and Function of the Atypical IκBs-Bcl-3, IκBEuropean journal of immunology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

23 authors at 8 institutions in 3 countries.

Takuya UehataDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0003-3517-2198
Shinnosuke YamadaDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Daisuke OriDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0002-2535-7837
Alexis VandenbonLaboratory of Tissue Homeostasis, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.ORCID 0000-0003-2180-5732
Amir GiladiDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.ORCID 0000-0002-5880-2845
Adam JelinskiDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Yasuhiro MurakawaInstitute for the Advanced Study of Human Biology, Kyoto University, Kyoto, Japan.
Hitomi WatanabeLaboratory of Integrative Biological Sciences, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.
Kazuhiro TakeuchiInstitute for the Advanced Study of Human Biology, Kyoto University, Kyoto, Japan.ORCID 0000-0002-1646-9167
Kazunori TorataniDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Takashi MinoDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0002-9562-008X
Hisanori KiryuDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan.ORCID 0000-0003-3554-5353
Daron M StandleyDepartment of Genome Informatics, Genome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Tohru TsujimuraDepartment of Pathology, Hyogo College of Medicine, Hyogo, Japan.
Tomokatsu IkawaDivision of Immunology and Allergy, Research Institute for Biomedical Sciences, Tokyo University of Science, Chiba, Japan.
Gen KondohLaboratory of Integrative Biological Sciences, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.
Markus LandthalerRNA Biology and Posttranscriptional Regulation, Max Delbrück Center for Molecular Medicine Berlin, Berlin Institute for Molecular Systems Biology, Berlin, Germany.ORCID 0000-0002-1075-8734
Hiroshi KawamotoLaboratory of Immunology, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.
Hans-Reimer RodewaldDivision for Cellular Immunology, German Cancer Research Center, Heidelberg, Germany.
Ido AmitDepartment of Immunology, Weizmann Institute of Science, Rehovot, Israel.
Ryo YamamotoInstitute for the Advanced Study of Human Biology, Kyoto University, Kyoto, Japan.
Masaki MiyazakiLaboratory of Immunology, Institute for Life and Medical Sciences, Kyoto University, Kyoto, Japan.ORCID 0000-0002-9543-624X
Osamu TakeuchiDepartment of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.ORCID 0000-0002-1260-6232
Kyoto University · JPWeizmann Institute of Science · ILGerman Cancer Research Center · DEHyogo Medical University · JPMax Delbrück Center · DEThe University of Osaka · JPThe University of Tokyo · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

abstractRegulation of lineage biases in hematopoietic stem and progenitor cells (HSPCs) is pivotal for balanced hematopoietic output. However, little is known about the mechanism behind lineage choice in HSPCs. Here, we show that messenger RNA (mRNA) decay factors regnase-1 (Reg1; Zc3h12a) and regnase-3 (Reg3; Zc3h12c) are essential for determining lymphoid fate and restricting myeloid differentiation in HSPCs. Loss of Reg1 and Reg3 resulted in severe impairment of lymphopoiesis and a mild increase in myelopoiesis in the bone marrow. Single-cell RNA sequencing analysis revealed that Reg1 and Reg3 regulate lineage directions in HSPCs via the control of a set of myeloid-related genes. Reg1- and Reg3-mediated control of mRNA encoding Nfkbiz, a transcriptional and epigenetic regulator, was essential for balancing lymphoid/myeloid lineage output in HSPCs in vivo. Furthermore, single-cell assay for transposase-accessible chromatin sequencing analysis revealed that Reg1 and Reg3 control the epigenetic landscape on myeloid-related gene loci in early stage HSPCs via Nfkbiz. Consistently, an antisense oligonucleotide designed to inhibit Reg1- and Reg3-mediated Nfkbiz mRNA degradation primed hematopoietic stem cells toward myeloid lineages by enhancing Nfkbiz expression. Collectively, the collaboration between posttranscriptional control and chromatin remodeling by the Reg1/Reg3-Nfkbiz axis governs HSPC lineage biases, ultimately dictating the fate of lymphoid vs myeloid differentiation.

Indexed as

Bone MarrowHematopoietic Stem CellsCell DifferentiationCell LineageHematopoiesisRNA, MessengerRNA, Messenger

Identifiers

PMID37922454
PMCPMC10808253
OpenAlexW4388281609

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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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.