Evidence map›Paper›PMID 21199920›Full record

ArticleMolecular and cellular biology2011

The ARID family transcription factor bright is required for both hematopoietic stem cell and B lineage development.

Carol F Webb, James Bryant, Melissa Popowski, Laura Allred, Dongkoon Kim, June Harriss, Christian Schmidt, Cathrine A Miner, Kira Rose, Hwei-Ling Cheng and 2 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Genetic susceptibility ofGlobal medical genetics · 2025
    Article
  4. Article
  5. Regulation of HSC development and function by Lin28b.Frontiers in cell and developmental biology · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. PNAS nexus · 2024
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. The Role of LIN28-International journal of molecular sciences · 2020
    Review
  19. Article
  20. Review
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

12 authors at 3 institutions in 1 country.

Carol F WebbImmunobiology and Cancer Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73126, USA.
James Bryant
Melissa Popowski
Laura Allred
Dongkoon Kim
June Harriss
Christian Schmidt
Cathrine A Miner
Kira Rose
Hwei-Ling Cheng
Courtney Griffin
Philip W Tucker
The University of Texas at Austin · USOklahoma Medical Research Foundation · USHoward Hughes Medical Institute · 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 CA31534NCI NIH HHS R01 CA031534PHS HHS 044215
6 · The paper itself

Abstract

Bright/Arid3a has been characterized both as an activator of immunoglobulin heavy-chain transcription and as a proto-oncogene. Although Bright expression is highly B lineage stage restricted in adult mice, its expression in the earliest identifiable hematopoietic stem cell (HSC) population suggests that Bright might have additional functions. We showed that >99% of Bright(-/-) embryos die at midgestation from failed hematopoiesis. Bright(-/-) embryonic day 12.5 (E12.5) fetal livers showed an increase in the expression of immature markers. Colony-forming assays indicated that the hematopoietic potential of Bright(-/-) mice is markedly reduced. Rare survivors of lethality, which were not compensated by the closely related paralogue Bright-derived protein (Bdp)/Arid3b, suffered HSC deficits in their bone marrow as well as B lineage-intrinsic developmental and functional deficiencies in their peripheries. These include a reduction in a natural antibody, B-1 responses to phosphocholine, and selective T-dependent impairment of IgG1 class switching. Our results place Bright/Arid3a on a select list of transcriptional regulators required to program both HSC and lineage-specific differentiation.

Indexed as

AnimalsAntibodiesB-LymphocytesCell LineageDNA-Binding ProteinsFemaleGene Expression Regulation, DevelopmentalGenes, LethalHematopoiesisHematopoietic Stem CellsImmunoglobulin Class SwitchingLymphopoiesisMaleMiceMice, Inbred C57BLPhosphorylcholineAntibodiesArid3a protein, mouseDNA-Binding ProteinsPhosphorylcholineTranscription Factors

Identifiers

PMID21199920
PMCPMC3067827
OpenAlexW2127381886

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.