Evidence map›Paper›PMID 27507669›Full record

ReviewMechanisms of ageing and development2017

ER fatalities-The role of ER-mitochondrial contact sites in yeast life and death decisions.

Daniel G J Smethurst, Katrina F Cooper

Abstract readReview
In one paragraph

Review in Mechanisms of ageing and development, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. 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.

Daniel G J SmethurstDepartment of Molecular Biology, Rowan University School of Osteopathic Medicine, Stratford, NJ, 08055 USA.
Katrina F CooperDepartment of Molecular Biology, Rowan University School of Osteopathic Medicine, Stratford, NJ, 08055 USA. Electronic address: cooperka@rowan.edu.

Funding

Stress regulated mitochondrial dynamicsR01GM113052 · NIGMS · ROWAN UNIVERSITY SCHOOL/OSTEOPATHIC MED · PI STRICH, RANDY S · 2014 to 2017
$1.3M
Stress induced signaling and cyclin C regulation in yeastR15GM113196 · NIGMS · ROWAN UNIVERSITY SCHOOL/OSTEOPATHIC MED · PI COOPER, KATRINA FRANCES · 2015 to 2015
$396k
NIGMS NIH HHS R01 GM113052NIGMS NIH HHS R15 GM113196
6 · The paper itself

Abstract

Following extracellular stress signals, all eukaryotic cells choose whether to elicit a pro-survival or pro-death response. The decision over which path to take is governed by the severity and duration of the damage. In response to mild stress, pro-survival programs are initiated (unfolded protein response, autophagy, mitophagy) whereas severe or chronic stress forces the cell to abandon these adaptive programs and shift towards regulated cell death to remove irreversibly damaged cells. Both pro-survival and pro-death programs involve regulated communication between the endoplasmic reticulum (ER) and mitochondria. In yeast, recent data suggest this inter-organelle contact is facilitated by the endoplasmic reticulum mitochondria encounter structure (ERMES). These membrane contacts are not only important for the exchange of cellular signals, but also play a role in mitochondrial tethering during mitophagy, mitochondrial fission and mitochondrial inheritance. This review focuses on recent findings in yeast that shed light on how ER-mitochondrial communication mediates critical cell fate decisions.

Indexed as

AutophagyEndoplasmic ReticulumMitochondriaMitophagySaccharomyces cerevisiaeUnfolded Protein ResponseEndoplasmic reticulumERMESMitochondriaMitophagyProgrammed cell deathSignal transduction

Identifiers

PMID27507669
PMCPMC5293681

What OpenQuestion holds

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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.