Evidence map›Paper›PMID 16738337›Full record

ArticleMolecular and cellular biology2006

Induction of immunoglobulin heavy-chain transcription through the transcription factor Bright requires TFII-I.

Jaya Rajaiya, Jamee C Nixon, Neil Ayers, Zana P Desgranges, Ananda L Roy, Carol F Webb

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

38 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  3. Review
  4. Article
  5. Article
  6. Article
  7. Regulation of B-cell function by NF-kappaB c-Rel in health and disease.Cellular and molecular life sciences : CMLS · 2020
    Review
  8. Article
  9. Review
  10. Observational
  11. Association ofNeural regeneration research · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

6 authors at 2 institutions in 1 country.

Jaya RajaiyaOklahoma Medical Research Foundation, Immunobiology and Cancer Research Program, 825 N. E. 13th Street, Oklahoma City, OK 73104, USA.
Jamee C Nixon
Neil Ayers
Zana P Desgranges
Ananda L Roy
Carol F Webb
Oklahoma Medical Research Foundation · USTufts University · 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
POTENTIAL ROLE OF TFII-I IN IMMUNODEFICIENCYR01AI045150 · NIAID · TUFTS UNIVERSITY BOSTON · PI ROY, ANANDA L · 2000 to 2004
$1.5M
Potential Role of TFII-I in ImmunodeficiencyR56AI045150 · NIAID · TUFTS UNIVERSITY BOSTON · PI ROY, ANANDA L · 2006 to 2006
$300k
IMMUNOBIOLOGY, CANCER, AND ARTHRITIS LABORATORIESC06RR014570 · NCRR · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI CAPRA, J DONALD · 1999 to 1999
–
NCRR NIH HHS C06 RR014570NCRR NIH HHS C06 RR14570-01NIAID NIH HHS AI044215NIAID NIH HHS AI45150NIAID NIH HHS R01 AI044215NIAID NIH HHS R01 AI045150NIAID NIH HHS R56 AI045150NIAID NIH HHS T32 AI007633
6 · The paper itself

Abstract

Bright/ARID3a/Dril1, a member of the ARID family of transcription factors, is expressed in a highly regulated fashion in B lymphocytes, where it enhances immunoglobulin transcription three- to sixfold. Recent publications from our lab indicated that functional, but not kinase-inactive, Bruton's tyrosine kinase (Btk) is critical for Bright activity in an in vitro model system, yet Bright itself is not appreciably tyrosine phosphorylated. These data suggested that a third protein, and Btk substrate, must contribute to Bright-enhanced immunoglobulin transcription. The ubiquitously expressed transcription factor TFII-I was identified as a substrate for Btk several years ago. In this work, we show that TFII-I directly interacts with human Bright through amino acids in Bright's protein interaction domain and that specific tyrosine residues of TFII-I are essential for Bright-induced activity of an immunoglobulin reporter gene. Moreover, inhibition of TFII-I function in a B-cell line resulted in decreased heavy-chain transcript levels. These data suggest that Bright functions as a three-component protein complex in the immunoglobulin locus and tie together previous data indicating important roles for Btk and TFII-I in B lymphocytes.

Indexed as

Genes, ImmunoglobulinAgammaglobulinaemia Tyrosine KinaseAnimalsBase SequenceBinding SitesB-LymphocytesCell LineDNA-Binding ProteinsHumansImmunoglobulin Heavy ChainsMiceMutationOncogenesProtein Structure, TertiaryProtein-Tyrosine KinasesRNA, MessengerAgammaglobulinaemia Tyrosine KinaseARID3A protein, humanBTK protein, humanBtk protein, mouseDNA-Binding ProteinsGTF2I protein, humanImmunoglobulin Heavy ChainsProtein-Tyrosine KinasesRNA, MessengerTrans-ActivatorsTranscription FactorsTranscription Factors, TFII

Identifiers

PMID16738337
PMCPMC1489113
OpenAlexW2124102632

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.