Evidence map›Paper›PMID 23823868›Full record

ArticlePLoS biology2013

Control of cellular Bcl-xL levels by deamidation-regulated degradation.

So Hee Dho, Benjamin E Deverman, Carlo Lapid, Scott R Manson, Lu Gan, Jacob J Riehm, Rajeev Aurora, Ki-Sun Kwon, Steven J Weintraub

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

20 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. BCL-2 and BCL-xL in Cancer: Regulation, Function, and Therapeutic Targeting.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. BCL-xL, a Mitochondrial Protein Involved in Successful Aging: FromInternational journal of molecular sciences · 2020
    Review
  8. Article
  9. Review
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  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
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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

9 authors at 5 institutions in 2 countries.

So Hee DhoDivision of Urology and The Alvin J. Siteman Cancer Center, Washington University School of Medicine, Saint Louis, Missouri, United States of America.
Benjamin E Deverman
Carlo Lapid
Scott R Manson
Lu Gan
Jacob J Riehm
Rajeev Aurora
Ki-Sun Kwon
Steven J Weintraub
Alvin J. Siteman Cancer CenterJohn Cochran VA Medical Center · USKorea Research Institute of Bioscience and Biotechnology · KRSaint Louis University · USWashington University in St. Louis · US

Funding

TRAINING PROGRAM IN CELLULAR AND MOLECULAR BIOLOGYT32GM007067 · NIGMS · WASHINGTON UNIVERSITY · PI TRUE-KROB, HEATHER L · 1985 to 2020
$20.4M
6 · The paper itself

Abstract

The cellular concentration of Bcl-xL is among the most important determinants of treatment response and overall prognosis in a broad range of tumors as well as an important determinant of the cellular response to several forms of tissue injury. We and others have previously shown that human Bcl-xL undergoes deamidation at two asparaginyl residues and that DNA-damaging antineoplastic agents as well as other stimuli can increase the rate of deamidation. Deamidation results in the replacement of asparginyl residues with aspartyl or isoaspartyl residues. Thus deamidation, like phosphorylation, introduces a negative charge into proteins. Here we show that the level of human Bcl-xL is constantly modulated by deamidation because deamidation, like phosphorylation in other proteins, activates a conditional PEST sequence to target Bcl-xL for degradation. Additionally, we show that degradation of deamidated Bcl-xL is mediated at least in part by calpain. Notably, we present sequence and biochemical data that suggest that deamidation has been conserved from the simplest extant metazoans through the human form of Bcl-xL, underscoring its importance in Bcl-xL regulation. Our findings strongly suggest that deamidation-regulated Bcl-xL degradation is an important component of the cellular rheostat that determines susceptibility to DNA-damaging agents and other death stimuli.

Indexed as

ProteolysisAmidesAmino Acid SequenceAnimalsbcl-X ProteinCalpainCell LineConserved SequenceDNA DamageHumansHydrogen-Ion ConcentrationMiceMolecular Sequence DataProtein Structure, TertiaryAmidesbcl-X ProteinCalpain

Identifiers

PMID23823868
PMCPMC3692414
OpenAlexW2113154740

What OpenQuestion holds

Textmetadata
LicenceCC0
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.