Evidence map›Paper›PMID 26431568›Full record

ReviewCurrent topics in developmental biology2015

Regulation of Cell Death by IAPs and Their Antagonists.

Deepika Vasudevan, Hyung Don Ryoo

Open access · greenAbstract readReview
In one paragraph

Review in Current topics in developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
12.4field-weighted citation impact, top 1% 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

34 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Apoptosis inhibition restrains primary malignant traits in differentFrontiers in cell and developmental biology · 2022
    Article
  11. Review
  12. The Duality of Caspases in Cancer, as Told through the Fly.International journal of molecular sciences · 2021
    Review
  13. Review
  14. A Look intoViruses · 2021
    Review
  15. Review
  16. Evolutionary novelty in the apoptotic pathway of aphids.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  17. Article
  18. Pro-Apoptotic Function Analysis of the Reaper Homologue IBM1 inInternational journal of molecular sciences · 2020
    Article
  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

2 authors at 1 institution in 1 country.

Deepika VasudevanDepartment of Cell Biology, New York University School of Medicine, New York, New York, USA.
Hyung Don RyooDepartment of Cell Biology, New York University School of Medicine, New York, New York, USA. Electronic address: hyungdon.ryoo@nyumc.org.
New York University · US

Funding

Unfolded Protein Response in Eye Development and DiseaseR01EY020866 · NEI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HYUNG D RYOO · 2010 to 2026
$6.9M
NEI NIH HHS R01 EY020866
6 · The paper itself

Abstract

Inhibitors of apoptosis (IAPs) family of genes encode baculovirus IAP-repeat domain-containing proteins with antiapoptotic function. These proteins also contain RING or UBC domains and act by binding to major proapoptotic factors and ubiquitylating them. High levels of IAPs inhibit caspase-mediated apoptosis. For these cells to undergo apoptosis, IAP function must be neutralized by IAP-antagonists. Mammalian IAP knockouts do not exhibit obvious developmental phenotypes, but the cells are more sensitized to apoptosis in response to injury. Loss of the mammalian IAP-antagonist ARTS results in reduced stem cell apoptosis. In addition to the antiapoptotic properties, IAPs regulate the innate immune response, and the loss of IAP function in humans is associated with immunodeficiency. The roles of IAPs in Drosophila apoptosis regulation are more apparent, where the loss of IAP1, or the expression of IAP-antagonists in Drosophila cells, is sufficient to trigger apoptosis. In this organism, apoptosis as a fate is conferred by the transcriptional induction of the IAP-antagonists. Many signaling pathways often converge on shared enhancer regions of IAP-antagonists. Cell death sensitivity is further regulated by posttranscriptional mechanisms, including those regulated by kinases, miRs, and ubiquitin ligases. These mechanisms are employed to eliminate damaged or virus-infected cells, limit neuroblast (neural stem cell) numbers, generate neuronal diversity, and sculpt tissue morphogenesis.

Indexed as

Cell DeathAnimalsApoptosisApoptosis Regulatory ProteinsCell MovementCell ProliferationDrosophila ProteinsGene Expression RegulationImmunity, InnateInhibitor of Apoptosis ProteinsMammalsMitochondriaMorphogenesisNervous SystemApoptosis Regulatory ProteinsDrosophila ProteinsInhibitor of Apoptosis ProteinsApoptosisARTSBRUCEc-IAP1DIAP1HIDIAP-antagonistREAPERSMACXIAP

Identifiers

PMID26431568
PMCPMC4861076
OpenAlexW2280301780

What OpenQuestion holds

Textmetadata
LicenceTDM
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.