Evidence map›Paper›PMID 25344725›Full record

ArticleNature immunology2014

The transcription repressors Bach2 and Bach1 promote B cell development by repressing the myeloid program.

Ari Itoh-Nakadai, Reina Hikota, Akihiko Muto, Kohei Kometani, Miki Watanabe-Matsui, Yuki Sato, Masahiro Kobayashi, Atsushi Nakamura, Yuichi Miura, Yoko Yano and 6 more

Abstract read
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In one paragraph

Article in Nature immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.

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24 more citing papers are in PubMed but not listed here.

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

16 authors at 4 institutions in 1 country.

Ari Itoh-Nakadai1] Department of Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan. [2] CREST, Japan Science and Technology Agency, Sendai, Japan.
Reina HikotaDepartment of Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan.
Akihiko Muto1] Department of Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan. [2] CREST, Japan Science and Technology Agency, Sendai, Japan.
Kohei KometaniRIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Miki Watanabe-MatsuiDepartment of Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan.
Yuki SatoDepartment of Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan.
Masahiro KobayashiDepartment of Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan.
Atsushi NakamuraDepartment of Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan.
Yuichi MiuraDepartment of Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan.
Yoko YanoDepartment of Cellular Biology, Research Institute for Radiation Biology and Medicine, Graduate School of Biomedical Science, Hiroshima University, Hiroshima, Japan.
Satoshi TashiroDepartment of Cellular Biology, Research Institute for Radiation Biology and Medicine, Graduate School of Biomedical Science, Hiroshima University, Hiroshima, Japan.
Jiying SunDepartment of Cellular Biology, Research Institute for Radiation Biology and Medicine, Graduate School of Biomedical Science, Hiroshima University, Hiroshima, Japan.
Tomokatsu IkawaLaboratory for Immune Regeneration RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Kyoko Ochiai1] Department of Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan. [2] CREST, Japan Science and Technology Agency, Sendai, Japan. [3] Center for Regulatory Epigenome and Diseases, Tohoku University Graduate School of Medicine, Sendai, Japan.
Tomohiro Kurosaki1] RIKEN Center for Integrative Medical Sciences, Yokohama, Japan. [2] WPI Immunology Frontier Research Center, Osaka University, Suita, Japan.
Kazuhiko Igarashi1] Department of Biochemistry, Tohoku University Graduate School of Medicine, Sendai, Japan. [2] CREST, Japan Science and Technology Agency, Sendai, Japan. [3] Center for Regulatory Epigenome and Diseases, Tohoku University Graduate School of Medicine, Sendai, Japan.
Tohoku University · JPHiroshima University · JPRIKEN Center for Integrative Medical Sciences · JPJapan Science and Technology Agency · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mature lymphoid cells express the transcription repressor Bach2, which imposes regulation on humoral and cellular immunity. Here we found critical roles for Bach2 in the development of cells of the B lineage, commencing from the common lymphoid progenitor (CLP) stage, with Bach1 as an auxiliary. Overexpression of Bach2 in pre-pro-B cells deficient in the transcription factor EBF1 and single-cell analysis of CLPs revealed that Bach2 and Bach1 repressed the expression of genes important for myeloid cells ('myeloid genes'). Bach2 and Bach1 bound to presumptive regulatory regions of the myeloid genes. Bach2(hi) CLPs showed resistance to myeloid differentiation even when cultured under myeloid conditions. Our results suggest that Bach2 functions with Bach1 and EBF1 to promote B cell development by repressing myeloid genes in CLPs.

Indexed as

AnimalsBasic-Leucine Zipper Transcription FactorsB-LymphocytesCell DifferentiationCell LineageCell SeparationChromatin ImmunoprecipitationElectrophoretic Mobility Shift AssayFlow CytometryGene Expression RegulationLymphoid Progenitor CellsLymphopoiesisMiceMice, Inbred C57BLMice, KnockoutOligonucleotide Array Sequence AnalysisBach1 protein, mouseBach2 protein, mouseBasic-Leucine Zipper Transcription FactorsEbf1 protein, mouseTrans-Activators

Identifiers

PMID25344725
OpenAlexW2087788999

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.