Evidence map›Paper›PMID 27515252›Full record

ArticleScientific reports2016

Regulation of B cell differentiation by the ubiquitin-binding protein TAX1BP1.

Nobuko Matsushita, Midori Suzuki, Emi Ikebe, Shun Nagashima, Ryoko Inatome, Kenichi Asano, Masato Tanaka, Masayuki Matsushita, Eisaku Kondo, Hidekatsu Iha and 1 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

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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

11 authors at 4 institutions in 1 country.

Nobuko MatsushitaLaboratory of Molecular Biochemistry, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan.
Midori SuzukiLaboratory of Molecular Biochemistry, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan.
Emi IkebeDepartment of Microbiology, Oita University Faculty of Medicine, Yufu, Oita, 879-5593, Japan.
Shun NagashimaLaboratory of Molecular Biochemistry, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan.
Ryoko InatomeLaboratory of Molecular Biochemistry, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan.
Kenichi AsanoLaboratory of Immune Regulation, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan.
Masato TanakaLaboratory of Immune Regulation, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan.
Masayuki MatsushitaDepartment of Molecular and Cellular Physiology, Graduate School of Medicine, University of the Ryukyus, Okinawa, 903-0215, Japan.
Eisaku KondoDivision of Molecular and Cellular Pathology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, 951-8510, Japan.
Hidekatsu IhaDepartment of Microbiology, Oita University Faculty of Medicine, Yufu, Oita, 879-5593, Japan.
Shigeru YanagiLaboratory of Molecular Biochemistry, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan.
Tokyo University of Pharmacy and Life Sciences · JPOita University · JPNiigata University · JPUniversity of the Ryukyus · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tax1-binding protein 1 (TAX1BP1) is a ubiquitin-binding protein that restricts nuclear factor-κB (NF-κB) activation and facilitates the termination of aberrant inflammation. However, its roles in B-cell activation and differentiation are poorly understood. To evaluate the function of TAX1BP1 in B cells, we established TAX1BP1-deficient DT40 B cells that are hyper-responsive to CD40-induced extracellular signal-regulated kinase (ERK) activation signaling, exhibit prolonged and exaggerated ERK phosphorylation and show enhanced B lymphocyte-induced maturation protein 1 (Blimp-1; a transcription factor inducing plasma cell differentiation) expression that is ERK-dependent. Furthermore, TAX1BP1-deficient cells exhibit significantly decreased surface IgM expression and increased IgM secretion. Moreover, TAX1BP1-deficient mice display reduced germinal center formation and antigen-specific antibody production. These findings show that TAX1BP1 restricts ERK activation and Blimp-1 expression and regulates germinal center formation.

Indexed as

AnimalsB-LymphocytesCell DifferentiationCell LineChickensExtracellular Signal-Regulated MAP KinasesGerminal CenterImmunoglobulin MIntracellular Signaling Peptides and ProteinsMaleMiceMice, KnockoutNeoplasm ProteinsPositive Regulatory Domain I-Binding Factor 1Extracellular Signal-Regulated MAP KinasesImmunoglobulin MIntracellular Signaling Peptides and ProteinsNeoplasm ProteinsPositive Regulatory Domain I-Binding Factor 1Prdm1 protein, mouseTAX1BP1 protein, mouse

Identifiers

PMID27515252
PMCPMC4981851
OpenAlexW2514323982

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.