Evidence map›Paper›PMID 25857523›Full record

ArticleNature communications2015

Mitochondrial function provides instructive signals for activation-induced B-cell fates.

Kyoung-Jin Jang, Hiroto Mano, Koji Aoki, Tatsunari Hayashi, Akihiko Muto, Yukiko Nambu, Katsu Takahashi, Katsuhiko Itoh, Shigeru Taketani, Stephen L Nutt and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

109 citing papers in PubMed, 190 citations in OpenAlex.

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  13. Mitochondrial metabolism and cancer therapeutic innovation.Signal transduction and targeted therapy · 2025
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49 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

13 authors at 7 institutions in 2 countries.

Kyoung-Jin JangDepartment of Experimental Therapeutics, Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Hiroto ManoDepartment of Experimental Therapeutics, Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Koji AokiDivision of Pharmacology, School of Medicine, University of Fukui, 23-3 Matsuokashimoaizuki, Eiheiji-cho, Yoshida-gun, Fukui 910-1193, Japan.
Tatsunari HayashiDepartment of Experimental Therapeutics, Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Akihiko Muto1] Department of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Aoba-ku, Sendai, Miyagi 980-8575, Japan [2] CREST, Japan Science and Technology Agency, Seiryo-machi 2-1, Aoba-ku, Sendai, Miyagi 980-8575, Japan.
Yukiko NambuDepartment of Experimental Therapeutics, Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Katsu TakahashiDepartment of Oral and Maxillofacial Surgery, Kyoto University Hospital, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Katsuhiko ItohDepartment of Clinical Molecular Biology, Graduate School of Medicine, Kyoto University, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Shigeru TaketaniDepartment of Biotechnology, Kyoto Institute of Technology, Matsugasaki, Sakyo-ku, Kyoto 606-8585, Japan.
Stephen L Nutt1] The Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria 3052, Australia [2] Department of Medical Biology, University of Melbourne, Victoria 3010, Australia.
Kazuhiko Igarashi1] Department of Biochemistry, Tohoku University Graduate School of Medicine, Seiryo-machi 2-1, Aoba-ku, Sendai, Miyagi 980-8575, Japan [2] CREST, Japan Science and Technology Agency, Seiryo-machi 2-1, Aoba-ku, Sendai, Miyagi 980-8575, Japan.
Akira ShimizuDepartment of Experimental Therapeutics, Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.
Manabu Sugai1] Department of Experimental Therapeutics, Institute for Advancement of Clinical and Translational Science, Kyoto University Hospital, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan [2] Division of Molecular Genetics, Department of Biochemistry and Bioinformative Sciences, School of Medicine, University of Fukui, 23-3 Matsuokashimoaizuki, Eiheiji-cho, Yoshida-gun, Fukui 910-1193, Japan.
Kyoto University Hospital · JPUniversity of Fukui · JPJapan Science and Technology Agency · JPKyoto Institute of Technology · JPKyoto University · JPTohoku University · JPWalter and Eliza Hall Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During immune reactions, functionally distinct B-cell subsets are generated by stochastic processes, including class-switch recombination (CSR) and plasma cell differentiation (PCD). In this study, we show a strong association between individual B-cell fates and mitochondrial functions. CSR occurs specifically in activated B cells with increased mitochondrial mass and membrane potential, which augment mitochondrial reactive oxygen species (mROS), whereas PCD occurs in cells with decreased mitochondrial mass and potential. These events are consequences of initial slight changes in mROS in mitochondria(high) B-cell populations. In CSR-committed cells, mROS attenuates haeme synthesis by inhibiting ferrous ion addition to protoporphyrin IX, thereby maintaining Bach2 function. Reduced mROS then promotes PCD by increasing haeme synthesis. In PCD-committed cells, Blimp1 reduces mitochondrial mass, thereby reducing mROS levels. Identifying mROS as a haeme synthesis regulator increases the understanding of mechanisms regulating haeme homeostasis and cell fate determination after B-cell activation.

Indexed as

Signal TransductionAnimalsBasic-Leucine Zipper Transcription FactorsB-Lymphocyte SubsetsCell DifferentiationCell TrackingGene ExpressionHemeImmunoglobulin Class SwitchingLymphocyte ActivationMaleMembrane Potential, MitochondrialMiceMice, Inbred C57BLMice, KnockoutMitochondriaBach2 protein, mouseBasic-Leucine Zipper Transcription FactorsHemePositive Regulatory Domain I-Binding Factor 1Prdm1 protein, mouseprotoporphyrin IXProtoporphyrinsReactive Oxygen SpeciesTranscription Factors

Identifiers

PMID25857523
PMCPMC4403446
OpenAlexW2166600785

What OpenQuestion holds

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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.