Evidence map›Paper›PMID 18477482›Full record

ReviewBiochimica et biophysica acta2008

Mitochondrial death pathways in yeast and mammalian cells.

Wen-Chih Cheng, Kelly M Leach, J Marie Hardwick

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Yeast for virus research.Microbial cell (Graz, Austria) · 2017
    Review
  12. Article
  13. Article
  14. Article
  15. Quantification of genetically controlled cell death in budding yeast.Methods in molecular biology (Clifton, N.J.) · 2013
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Gene-dependent cell death in yeast.Cell death & disease · 2011
    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

3 authors at 1 institution in 1 country.

Wen-Chih ChengW Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, MD 21205, USA.
Kelly M Leach
J Marie Hardwick
Johns Hopkins University · US

Funding

REGULATION OF BCL XL BY CASPASESR01NS037402 · NINDS · JOHNS HOPKINS UNIVERSITY · PI HARDWICK, J. MARIE · 1999 to 2014
$4.5M
REGULATION OF VIRAL INFECTIONS BY CELLULAR GENESR01NS034175 · NINDS · JOHNS HOPKINS UNIVERSITY · PI HARDWICK, J. MARIE · 1995 to 2009
$2.5M
Conserved Cell Death Pathways in Mammals and YeastR01GM077875 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI HARDWICK, J. MARIE · 2006 to 2010
$1.4M
NIGMS NIH HHS GM 077875NIGMS NIH HHS R01 GM077875NINDS NIH HHS NS 34175NINDS NIH HHS R01 NS034175NINDS NIH HHS R01 NS037402
6 · The paper itself

Abstract

In mammals, mitochondria are important mediators of programmed cell death, and this process is often regulated by Bcl-2 family proteins. However, a role for mitochondria-mediated cell death in non-mammalian species is more controversial. New evidence from a variety of sources suggests that mammalian mitochondrial fission/division proteins also have the capacity to promote programmed cell death, which may involve interactions with Bcl-2 family proteins. Homologues of these fission factors and several additional mammalian cell death regulators are conserved in flies, worms and yeast, and have been suggested to regulate programmed cell death in these species as well. However, the molecular mechanisms by which these phylogenetically conserved proteins contribute to cell death are not known for any species. Some have taken the conserved pro-death activity of mitochondrial fission factors to mean that mitochondrial fission per se, or failed attempts to undergo fission, are directly involved in cell death. Other evidence suggests that the fission function and the cell death function of these factors are separable. Here we consider the evidence for these arguments and their implications regarding the origins of programmed cell death.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsMammalsMitochondriaProto-Oncogene Proteins c-bcl-2YeastsApoptosis Regulatory ProteinsProto-Oncogene Proteins c-bcl-2

Identifiers

PMID18477482
PMCPMC2519237
OpenAlexW2106145727

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.