Evidence map›Paper›PMID 26431562›Full record

ReviewCurrent topics in developmental biology2015

Cell Death in C. elegans Development.

Jennifer Zuckerman Malin, Shai Shaham

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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.7field-weighted citation impact, top 3% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. A Compilation of the Diverse miRNA Functions inInternational journal of molecular sciences · 2023
    Review
  10. Article
  11. Autophagic Cell Death During Development - Ancient and Mysterious.Frontiers in cell and developmental biology · 2021
    Review
  12. Cell death in animal development.Development (Cambridge, England) · 2020
    Review
  13. Article
  14. Review
  15. C. elegans as a model in developmental neurotoxicology.Toxicology and applied pharmacology · 2018
    Review
  16. Article
  17. Article
  18. Article
  19. Frailty andFrontiers in nutrition · 2018
    Review
  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

2 authors at 1 institution in 1 country.

Jennifer Zuckerman MalinLaboratory of Developmental Genetics, The Rockefeller University, New York, USA.
Shai ShahamLaboratory of Developmental Genetics, The Rockefeller University, New York, USA. Electronic address: shaham@rockefeller.edu.
Rockefeller University · US

Funding

Control of nonapoptotic C. elegans cell death similar to neurodegenerationR01NS081490 · NINDS · ROCKEFELLER UNIVERSITY · PI SHAHAM, SHAI · 2012 to 2017
$2.2M
Control of Linker Cell Death in C. elegansR01HD078703 · NICHD · ROCKEFELLER UNIVERSITY · PI SHAHAM, SHAI · 2014 to 2018
$1.7M
NICHD NIH HHS HD078703NICHD NIH HHS R01 HD078703NINDS NIH HHS NS081490NINDS NIH HHS R01 NS081490
6 · The paper itself

Abstract

Cell death is a common and important feature of animal development, and cell death defects underlie many human disease states. The nematode Caenorhabditis elegans has proven fertile ground for uncovering molecular and cellular processes controlling programmed cell death. A core pathway consisting of the conserved proteins EGL-1/BH3-only, CED-9/BCL2, CED-4/APAF1, and CED-3/caspase promotes most cell death in the nematode, and a conserved set of proteins ensures the engulfment and degradation of dying cells. Multiple regulatory pathways control cell death onset in C. elegans, and many reveal similarities with tumor formation pathways in mammals, supporting the idea that cell death plays key roles in malignant progression. Nonetheless, a number of observations suggest that our understanding of developmental cell death in C. elegans is incomplete. The interaction between dying and engulfing cells seems to be more complex than originally appreciated, and it appears that key aspects of cell death initiation are not fully understood. It has also become apparent that the conserved apoptotic pathway is dispensable for the demise of the C. elegans linker cell, leading to the discovery of a previously unexplored gene program promoting cell death. Here, we review studies that formed the foundation of cell death research in C. elegans and describe new observations that expand, and in some cases remodel, this edifice. We raise the possibility that, in some cells, more than one death program may be needed to ensure cell death fidelity.

Indexed as

AnimalsApoptosisCaenorhabditis elegansCaenorhabditis elegans ProteinsCalcium-Binding ProteinsCaspasesCell DeathGene Expression RegulationProto-Oncogene Proteins c-bcl-2Repressor ProteinsCaenorhabditis elegans ProteinsCalcium-Binding ProteinsCaspasesced-3 protein, C elegansCed-4 protein, C elegansCed-9 protein, C elegansEGL-1 protein, C elegansProto-Oncogene Proteins c-bcl-2Repressor ProteinsApoptosisC. elegansCell deathLinker cellNonapoptotic cell death

Identifiers

PMID26431562
PMCPMC5206663
OpenAlexW2326698730

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.