Evidence map›Paper›PMID 28320875›Full record

ArticleMolecular and cellular biology2017

GATA3 Abundance Is a Critical Determinant of T Cell Receptor β Allelic Exclusion.

Chia-Jui Ku, JoAnn M Sekiguchi, Bharat Panwar, Yuanfang Guan, Satoru Takahashi, Keigyou Yoh, Ivan Maillard, Tomonori Hosoya, James Douglas Engel

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular and cellular biology, 2017. 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
0.4field-weighted citation impact, top 39% 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, 5 citations in OpenAlex.

  1. Article
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

9 authors at 2 institutions in 4 countries.

Chia-Jui KuDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan, USA.
JoAnn M SekiguchiDivision of Molecular Medicine and Genetics, Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Bharat PanwarDepartment of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan, USA.
Yuanfang GuanDepartment of Computational Medicine and Bioinformatics, University of Michigan, Ann Arbor, Michigan, USA.
Satoru TakahashiDepartment of Anatomy and Embryology, Faculty of Medicine, International Institute for Integrative Sleep Medicine (WPI-IIIS), Life Science Center, Tsukuba Advanced Research Alliance, and Laboratory Animal Resource Center, University of Tsukuba, Tsukaba, Japan.
Keigyou YohDepartment of Anatomy and Embryology, Faculty of Medicine, International Institute for Integrative Sleep Medicine (WPI-IIIS), Life Science Center, Tsukuba Advanced Research Alliance, and Laboratory Animal Resource Center, University of Tsukuba, Tsukaba, Japan.
Ivan MaillardDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan, USA.
Tomonori HosoyaDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan, USA.
James Douglas EngelDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, Michigan, USA engel@umich.edu.
University of Michigan · USUniversity of Tsukuba · JP

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Alexey I Nesvizhskii · 1988 to 2026
$178.2M
Notch Signaling in AlloimmunityR01AI091627 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI PEAR, WARREN S · 2011 to 2025
$6.0M
Roles of the Artemis nuclease in DNA repair and diseaseR01AI063058 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SEKIGUCHI, JOANN · 2005 to 2013
$3.0M
GATA3 regulation in transcriptional networks during hematopoietic cell developmenR01AI094642 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ENGEL, JAMES DOUGLAS · 2012 to 2016
$1.9M
NCI NIH HHS P30 CA046592NIAID NIH HHS R01 AI063058NIAID NIH HHS R01 AI091627NIAID NIH HHS R01 AI094642
6 · The paper itself

Abstract

Allelic exclusion describes the essential immunological process by which feedback repression of sequential DNA rearrangements ensures that only one autosome expresses a functional T or B cell receptor. In wild-type mammals, approximately 60% of cells have recombined the DNA of one T cell receptor β (TCRβ) V-to-DJ-joined allele in a functional configuration, while the second allele has recombined only the DJ sequences; the other 40% of cells have recombined the V to the DJ segments on both alleles, with only one of the two alleles predicting a functional TCRβ protein. Here we report that the transgenic overexpression of GATA3 leads predominantly to biallelic TCRβ gene (

Indexed as

AllelesAnimalsGATA3 Transcription FactorGene Expression RegulationGene OntologyMice, Inbred C57BLMice, TransgenicModels, BiologicalMutationProtein BindingReceptors, Antigen, T-Cell, alpha-betaRNA, MessengerSequence Analysis, RNASpleenThymocytesV(D)J RecombinationGATA3 Transcription FactorReceptors, Antigen, T-Cell, alpha-betaRNA, Messengerallelic exclusionGATA3monoallelic-to-biallelic switchT cell receptor beta locus

Identifiers

PMID28320875
PMCPMC5452726
OpenAlexW2603803144

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.