Evidence map›Paper›PMID 28380071›Full record

ArticlePloS one2017

The abundance of the ARL2 GTPase and its GAP, ELMOD2, at mitochondria are modulated by the fusogenic activity of mitofusins and stressors.

Laura E Newman, Cara R Schiavon, Chengjing Zhou, Richard A Kahn

Open access · goldAbstract read
In one paragraph

Article in PloS one, 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
1.1field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Membrane trafficking alterations in breast cancer progression.Frontiers in cell and developmental biology · 2024
    Review
  5. The Arf family GTPases: Regulation of vesicle biogenesis and beyond.BioEssays : news and reviews in molecular, cellular and developmental biology · 2023
    Review
  6. Mitofusins: from mitochondria to fertility.Cellular and molecular life sciences : CMLS · 2022
    Review
  7. Article
  8. Roles for ELMOD2 and Rootletin in ciliogenesis.Molecular biology of the cell · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Compositional complexity of rods and rings.Molecular biology of the cell · 2018
    Article
  13. Article
  14. MicroRNA-195: a review of its role in cancers.OncoTargets and therapy · 2018
    Review
  15. Article
  16. 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

4 authors at 1 institution in 1 country.

Laura E NewmanDepartment of Biochemistry, Emory University School of Medicine, Atlanta, Georgia, United States of America.
Cara R SchiavonDepartment of Biochemistry, Emory University School of Medicine, Atlanta, Georgia, United States of America.
Chengjing ZhouDepartment of Biochemistry, Emory University School of Medicine, Atlanta, Georgia, United States of America.
Richard A KahnDepartment of Biochemistry, Emory University School of Medicine, Atlanta, Georgia, United States of America.
Emory University · US

Funding

ENNCF - Viral Vector CoreP30NS055077 · NINDS · EMORY UNIVERSITY · PI RESSLER, KERRY J. · 2008 to 2018
$6.8M
Molecular mechanisms of ARF family GTPasesR35GM122568 · NIGMS · EMORY UNIVERSITY · PI KAHN, RICHARD A · 2017 to 2024
$3.7M
The Regulation and Cellular Activities of the ARL2 GTPaseR01GM090158 · NIGMS · EMORY UNIVERSITY · PI KAHN, RICHARD A · 2010 to 2017
$2.5M
Regulation of mitochondrial function by ARL2 and its putative effector ELMOD2F31GM111047 · NIGMS · EMORY UNIVERSITY · PI NEWMAN, LAURA ELIZABETH · 2014 to 2017
$92k
NIGMS NIH HHS F31 GM111047NIGMS NIH HHS R01 GM090158NIGMS NIH HHS R35 GM122568NINDS NIH HHS P30 NS055077
6 · The paper itself

Abstract

Mitochondria are essential, dynamic organelles that respond to a number of stressors with changes in morphology that are linked to several mitochondrial functions, though the mechanisms involved are poorly understood. We show that the levels of the regulatory GTPase ARL2 and its GAP, ELMOD2, are specifically increased at mitochondria in immortalized mouse embryo fibroblasts deleted for Mitofusin 2 (MFN2), but not MFN1. Elevated ARL2 and ELMOD2 in MEFs deleted for MFN2 could be reversed by re-introduction of MFN2, but only when the mitochondrial fragmentation in these MEFs was also reversed, demonstrating that reversal of elevated ARL2 and ELMOD2 requires the fusogenic activity of MFN2. Other stressors with links to mitochondrial morphology were investigated and several, including glucose or serum deprivation, also caused increases in ARL2 and ELMOD2. In contrast, a number of pharmacological inhibitors of energy metabolism caused increases in ARL2 without affecting ELMOD2 levels. Together we interpret these data as evidence of two ARL2-sensitive pathways in mitochondria, one affecting ATP levels that is independent of ELMOD2 and the other leading to mitochondrial fusion involving MFN2 that does involve ELMOD2.

Indexed as

Adenosine TriphosphateAnimalsCytoskeletal ProteinsGene Knockdown TechniquesGlucoseGTP-Binding ProteinsGTP PhosphohydrolasesMiceMitochondriaMitochondrial DynamicsAdenosine TriphosphateArl2 protein, mouseCytoskeletal ProteinsELMOD2 protein, mouseGlucoseGTP-Binding ProteinsGTP PhosphohydrolasesMfn1 protein, mouseMfn2 protein, mouse

Identifiers

PMID28380071
PMCPMC5381910
OpenAlexW2604993250

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.