Evidence map›Paper›PMID 24678314›Full record

ReviewFrontiers in immunology2014

The Bright Side of Hematopoiesis: Regulatory Roles of ARID3a/Bright in Human and Mouse Hematopoiesis.

Michelle L Ratliff, Troy D Templeton, Julie M Ward, Carol F Webb

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

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  6. PNAS nexus · 2024
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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

4 authors at 2 institutions in 1 country.

Michelle L RatliffImmunobiology and Cancer Research, Oklahoma Medical Research Foundation , Oklahoma City, OK , USA.
Troy D TempletonDepartment of Cell Biology, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA.
Julie M WardDepartment of Microbiology and Immunology, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA.
Carol F WebbImmunobiology and Cancer Research, Oklahoma Medical Research Foundation , Oklahoma City, OK , USA ; Department of Cell Biology, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA ; Department of Microbiology and Immunology, University of Oklahoma Health Sciences Center , Oklahoma City, OK , USA.
Oklahoma Medical Research Foundation · USUniversity of Oklahoma Health Sciences Center · US

Funding

Molecular Basis of Immunity - Kirschtein-NRSAT32AI007633 · NIAID · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CUNNINGHAM, MADELEINE W. · 2001 to 2022
$4.0M
Bright Function in the Immune SystemR01AI044215 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI WEBB, CAROL F · 1999 to 2009
$2.4M
Role of the transcription factor ARID3a in lupusR21AI090343 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI WEBB, CAROL F · 2010 to 2011
$430k
NIAID NIH HHS R01 AI044215NIAID NIH HHS R21 AI090343NIAID NIH HHS T32 AI007633
6 · The paper itself

Abstract

ARID3a/Bright is a DNA-binding protein that was originally discovered for its ability to increase immunoglobulin transcription in antigen-activated B cells. It interacts with DNA as a dimer through its ARID, or A/T-rich interacting domain. In association with other proteins, ARID3a increased transcription of the immunoglobulin heavy chain and led to improved chromatin accessibility of the heavy chain enhancer. Constitutive expression of ARID3a in B lineage cells resulted in autoantibody production, suggesting its regulation is important. Abnormal ARID3a expression has also been associated with increased proliferative capacity and malignancy. Roles for ARID3a in addition to interactions with the immunoglobulin locus were suggested by transgenic and knockout mouse models. Over-expression of ARID3a resulted in skewing of mature B cell subsets and altered gene expression patterns of follicular B cells, whereas loss of function resulted in loss of B1 lineage B cells and defects in hematopoiesis. More recent studies showed that loss of ARID3a in adult somatic cells promoted developmental plasticity, alterations in gene expression patterns, and lineage fate decisions. Together, these data suggest new regulatory roles for ARID3a. The genes influenced by ARID3a are likely to play pivotal roles in lineage decisions, highlighting the importance of this understudied transcription factor.

Indexed as

ARID3aB cell developmentBrightgene regulationhematopoietic regulation

Identifiers

PMID24678314
PMCPMC3958700
OpenAlexW2146863592

What OpenQuestion holds

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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.