Evidence map›Paper›PMID 21955986›Full record

ArticleMolecular immunology2011

Characterization of a new ARID family transcription factor (Brightlike/ARID3C) that co-activates Bright/ARID3A-mediated immunoglobulin gene transcription.

Josephine A Tidwell, Christian Schmidt, Phillip Heaton, Van Wilson, Philip W Tucker

Open access · greenAbstract read
In one paragraph

Article in Molecular immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

20 citing papers in PubMed, 25 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

5 authors at 2 institutions in 1 country.

Josephine A TidwellInstitute for Cellular and Molecular Biology, Section of Molecular Genetics and Microbiology, The University of Texas at Austin, Austin, TX 78712, USA.
Christian Schmidt
Phillip Heaton
Van Wilson
Philip W Tucker
The University of Texas at Austin · USTexas A&M Health Science Center · US

Funding

MAR MEDIATED GENETIC SWITCH FOR IGH ENHANCER CONTROLR01CA031534 · NCI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI TUCKER, HALEY O · 1985 to 2012
$2.9M
NCI NIH HHS R01 CA031534PHS HHS CACA31534
6 · The paper itself

Abstract

Two members, Bright/ARID3A and Bdp/ARID3B, of the ARID (AT-Rich Interaction Domain) transcription family are distinguished by their ability to specifically bind to DNA and to self-associate via a second domain, REKLES. Bright and Bdp positively regulate immunoglobulin heavy chain gene (IgH) transcription by binding to AT-rich motifs within Matrix Associating Regions (MARs) residing within a subset of V(H) promoters and the Eμ intronic enhancer. In addition, REKLES provides Bright nuclear export function, and a small pool of Bright is directed to plasma membrane sub-domains/lipid rafts where it associates with and modulates signaling of the B cell antigen receptor (BCR). Here, we characterize a third, highly conserved, physically condensed ARID3 locus, Brightlike/ARID3C. Brightlike encodes two alternatively spliced, SUMO-I-modified isoforms that include or exclude (Δ6) the REKLES-encoding exon 6. Brightlike transcripts and proteins are expressed preferentially within B lineage lymphocytes and coordinate with highest Bright expression in activated follicular B cells. Brightlike, but not BrightlikeΔ6, undergoes nuclear-cytoplasmic shuttling with a fraction localizing within lipid rafts following BCR stimulation. Brightlike, but not BrightlikeΔ6, associates with Bright in solution, at common DNA binding sites in vitro, and is enriched at Bright binding sites in chromatin. Although possessing little transactivation capacity of its own, Brightlike significantly co-activates Bright-dependent IgH transcription with maximal activity mediated by the unsumoylated form. In sum, this report introduces Brightlike as an additional functional member of the family of ARID proteins, which should be considered in regulatory circuits, previously ascribed to be mediated by Bright.

Indexed as

Transcription, GeneticAnimalsBlotting, WesternB-LymphocytesCell LineCell SeparationChromatin ImmunoprecipitationDNA-Binding ProteinsElectrophoretic Mobility Shift AssayFlow CytometryGenes, Immunoglobulin Heavy ChainHumansImmunoprecipitationMembrane MicrodomainsMiceMutagenesis, Site-DirectedARID3A protein, humanARID3C protein, humanArid3c protein, mouseDNA-Binding ProteinsProtein IsoformsTrans-ActivatorsTranscription Factors

Identifiers

PMID21955986
PMCPMC3205283
OpenAlexW2005076521

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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.