Evidence map›Paper›PMID 15173209›Full record

ArticleThe Journal of experimental medicine2004

Surface mu heavy chain signals down-regulation of the V(D)J-recombinase machinery in the absence of surrogate light chain components.

Gunther R Galler, Cornelia Mundt, Mathew Parker, Roberta Pelanda, Inga-Lill Mårtensson, Thomas H Winkler

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Review
  6. Article
  7. Checkpoints that control B cell development.The Journal of clinical investigation · 2015
    Review
  8. Article
  9. Article
  10. Mechanism for pre-B cell loss in VH-mutant rabbits.Journal of immunology (Baltimore, Md. : 1950) · 2011
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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

6 authors at 3 institutions in 3 countries.

Gunther R GallerHematopoiesis Unit, Nikolaus-Fiebiger-Center, Friedrich-Alexander University, Glueckstrasse 6, 91054 Erlangen, Germany.
Cornelia Mundt
Mathew Parker
Roberta Pelanda
Inga-Lill Mårtensson
Thomas H Winkler
Babraham Institute · GBJustus-Liebig-Universität Gießen · DENational Jewish Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Early B cell development is characterized by stepwise, ordered rearrangement of the immunoglobulin (Ig) heavy (HC) and light (LC) chain genes. Only one of the two alleles of these genes is used to produce a receptor, a phenomenon referred to as allelic exclusion. It has been suggested that pre-B cell receptor (pre-BCR) signals are responsible for down-regulation of the VDJH-recombinase machinery (Rag1, Rag2, and terminal deoxynucleotidyl transferase [TdT]), thereby preventing further rearrangement on the second HC allele. Using a mouse model, we show that expression of an inducible muHC transgene in Rag2-/- pro-B cells induces down-regulation of the following: (a) TdT protein, (b) a transgenic green fluorescent protein reporter reflecting endogenous Rag2 expression, and (c) Rag1 primary transcripts. Similar effects were also observed in the absence of surrogate LC (SLC) components, but not in the absence of the signaling subunit Ig-alpha. Furthermore, in wild-type mice and in mice lacking either lambda5, VpreB1/2, or the entire SLC, the TdT protein is down-regulated in muHC+LC- pre-B cells. Surprisingly, muHC without LC is expressed on the surface of pro-/pre-B cells from lambda5-/-, VpreB1-/-VpreB2-/-, and SLC-/- mice. Thus, SLC or LC is not required for muHC cell surface expression and signaling in these cells. Therefore, these findings offer an explanation for the occurrence of HC allelic exclusion in mice lacking SLC components.

Indexed as

AllelesAnimalsB-LymphocytesDNA-Binding ProteinsDNA NucleotidylexotransferaseDown-RegulationHematopoietic Stem CellsHomeodomain ProteinsImmunoglobulin Light ChainsImmunoglobulin mu-ChainsMiceReceptors, Antigen, B-CellRecombination, GeneticVDJ RecombinasesDNA-Binding ProteinsDNA NucleotidylexotransferaseHomeodomain ProteinsImmunoglobulin Light ChainsImmunoglobulin mu-ChainsRAG-1 proteinRag2 protein, mouseReceptors, Antigen, B-CellVDJ RecombinasesV(D)J recombination activating protein 2

Identifiers

PMID15173209
PMCPMC2211789
OpenAlexW2108262871

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.