Evidence map›Paper›PMID 17318174›Full record

ArticleThe EMBO journal2007

Notch inhibits apoptosis by direct interference with XIAP ubiquitination and degradation.

Wen-Hsien Liu, Huey-Wen Hsiao, Wen-I Tsou, Ming-Zong Lai

Abstract readComparative Study
In one paragraph

Article in The EMBO journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
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

28 citing papers in PubMed.

  1. Notch2 Inhibition and Kidney Cyst Growth in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2025
    Article
  2. Review
  3. Article
  4. Article
  5. Infection and immunity · 2023
    Article
  6. lncRNAProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Notch controls the magnitude of T helper cell responses by promoting cellular longevity.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  18. Review
  19. Article
  20. 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

4 authors.

Wen-Hsien LiuInstitute of Molecular Biology, Academia Sinica, Taipei, Taiwan, ROC.
Huey-Wen Hsiao
Wen-I Tsou
Ming-Zong Lai

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The physiological activity of Notch is a function of its ability to increase survival in many cell types. Several pathways have been shown to contribute to the survival effect of Notch, but the exact mechanism of Notch action is not completely understood. Here we identified that the regulation of cell survival by Notch intracellular domain could partly be attributed to a selective increase of X-linked inhibitor of apoptosis protein (XIAP). We further found that Notch intracellular domain inhibited the degradation of XIAP during apoptosis. The transactivation domain of Notch interacted directly with the RING region of XIAP to block the binding of E2 and prevent the in vivo and in vitro ubiquitination of XIAP. This antiapoptotic activity of Notch was abolished when XIAP was knocked down. Our results reveal a novel mechanism for Notch-selective suppression of apoptosis through an increase in the stability of a key antiapoptotic protein, XIAP.

Indexed as

AnimalsApoptosisDensitometryDNA PrimersElectroporationFlow CytometryMiceReceptors, NotchReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingT-LymphocytesUbiquitinsX-Linked Inhibitor of Apoptosis ProteinDNA PrimersReceptors, NotchRNA, Small InterferingUbiquitinsX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID17318174
PMCPMC1829378

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.