Evidence map›Paper›PMID 22949502›Full record

ArticleMolecular and cellular biology2012

A novel mechanism for the autonomous termination of pre-B cell receptor expression via induction of lysosome-associated protein transmembrane 5.

Yohei Kawano, Rika Ouchida, Ji-Yang Wang, Soichiro Yoshikawa, Mutsumi Yamamoto, Daisuke Kitamura, Hajime Karasuyama

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. LAPTM5 mediates immature B cell apoptosis and B cell tolerance by regulating the WWP2-PTEN-AKT pathway.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  7. Article
  8. Article
  9. The Ig heavy chain protein but not its message controls early B cell development.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  10. Article
  11. Article
  12. Article
  13. 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

7 authors at 3 institutions in 1 country.

Yohei KawanoDepartment of Immune Regulation, Tokyo Medical and Dental University Graduate School, Tokyo, Japan.
Rika Ouchida
Ji-Yang Wang
Soichiro Yoshikawa
Mutsumi Yamamoto
Daisuke Kitamura
Hajime Karasuyama
Tokyo Medical and Dental University · JPRIKEN Center for Integrative Medical Sciences · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The expression of the pre-B cell receptor (BCR) is confined to the early stage of B cell development, and its dysregulation is associated with anomalies of B-lineage cells, including leukemogenesis. Previous studies suggested that the pre-BCR signal might trigger the autonomous termination of pre-BCR expression even before the silencing of pre-BCR gene expression to prevent sustained pre-BCR expression. However, the underlying mechanism remains ill defined. Here we demonstrate that the pre-BCR signal induces the expression of lysosome-associated protein transmembrane 5 (LAPTM5), which leads to the prompt downmodulation of the pre-BCR. While LAPTM5 induction had no significant impact on the internalization of cell surface pre-BCR, it elicited the translocation of a large pool of intracellular pre-BCR from the endoplasmic reticulum to the lysosomal compartment concomitantly with a drastic reduction of the level of intracellular pre-BCR proteins. This reduction was inhibited by lysosomal inhibitors, indicating the lysosomal degradation of the pre-BCR. Notably, the LAPTM5 deficiency in pre-B cells led to the augmented expression level of surface pre-BCR. Collectively, the pre-BCR induces the prompt downmodulation of its own expression through the induction of LAPTM5, which promotes the lysosomal transport and degradation of the intracellular pre-BCR pool and, hence, limits the supply of pre-BCR to the cell surface.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsB-LymphocytesCell LineCell MembraneDown-RegulationEndoplasmic ReticulumImmediate-Early ProteinsLymphocyte ActivationLysosomesMembrane ProteinsMiceMice, KnockoutPre-B Cell ReceptorsProtein TransportSignal TransductionAdaptor Proteins, Signal TransducingB cell linker proteinImmediate-Early ProteinsLaptm5 protein, mouseMembrane ProteinsPre-B Cell Receptors

Identifiers

PMID22949502
PMCPMC3486144
OpenAlexW2141149338

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.