Evidence map›Paper›PMID 27233284›Full record

ReviewCurrent genetics2017

Target of rapamycin signaling mediates vacuolar fragmentation.

Bobbiejane Stauffer, Ted Powers

Abstract readReview
In one paragraph

Review in Current genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
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  4. Article
  5. Review
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  11. Review
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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.

Bobbiejane StaufferDepartment of Molecular and Cellular Biology, College of Biological Sciences, University of California, Davis, One Shields Ave., Davis, CA, 95616, USA.
Ted PowersDepartment of Molecular and Cellular Biology, College of Biological Sciences, University of California, Davis, One Shields Ave., Davis, CA, 95616, USA. tpowers@ucdavis.edu.

Funding

TOR Complex 2 and sphingolipid biosynthesis.R01GM086387 · NIGMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI POWERS, TED · 2009 to 2012
$1.3M
NIGMS NIH HHS R01 GM086387
6 · The paper itself

Abstract

In eukaryotic cells, cellular homeostasis requires that different organelles respond to intracellular as well as environmental signals and modulate their behavior as conditions demand. Understanding the molecular mechanisms required for these changes remains an outstanding goal. One such organelle is the lysosome/vacuole, which undergoes alterations in size and number in response to environmental and physiological stimuli. Changes in the morphology of this organelle are mediated in part by the equilibrium between fusion and fission processes. While the fusion of the yeast vacuole has been studied intensively, the regulation of vacuolar fission remains poorly characterized by comparison. In recent years, a number of studies have incorporated genome-wide visual screens and high-throughput microscopy to identify factors required for vacuolar fission in response to diverse cellular insults, including hyperosmotic and endoplasmic reticulum stress. Available evidence now demonstrates that the rapamycin-sensitive TOR network, a master regulator of cell growth, is required for vacuolar fragmentation in response to stress. Importantly, many of the genes identified in these studies provide new insights into potential links between the vacuolar fission machinery and TOR signaling. Together these advances both extend our understanding of the regulation of vacuolar fragmentation in yeast as well as underscore the role of analogous events in mammalian cells.

Indexed as

Signal TransductionAnimalsBiological TransportGene Expression RegulationHumansIntracellular MembranesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesProtein BindingProtein TransportStress, PhysiologicalTOR Serine-Threonine KinasesVacuolesYeastsMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesTOR Serine-Threonine KinasesER stressTORC1Vacuolar fission

Identifiers

PMID27233284
PMCPMC5124550

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.