Evidence map›Paper›PMID 25531880›Full record

ArticlePloS one2014

mTORC2 is required for rit-mediated oxidative stress resistance.

Weikang Cai, Douglas A Andres

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. mTORC2: a multifaceted regulator of autophagy.Cell communication and signaling : CCS · 2023
    Review
  8. The mTOR signaling pathway in cardiac aging.The journal of cardiovascular aging · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. New mechanistic insights into the RAS-SIN1 interaction at the membrane.Frontiers in cell and developmental biology · 2022
    Article
  13. Article
  14. The role of mTOR in age-related diseases.Journal of enzyme inhibition and medicinal chemistry · 2021
    Review
  15. HJournal of fungi (Basel, Switzerland) · 2021
    Article
  16. Review
  17. Article
  18. The Roles of Post-Translational Modifications on mTOR Signaling.International journal of molecular sciences · 2021
    Review
  19. Expanding TOR Complex 2 Signaling: Emerging Regulators and New Connections.Frontiers in cell and developmental biology · 2021
    Review
  20. 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 at 1 institution in 1 country.

Weikang CaiDepartment of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, Kentucky, United States of America.
Douglas A AndresDepartment of Molecular and Cellular Biochemistry, University of Kentucky, Lexington, Kentucky, United States of America.
University of Kentucky · US

Funding

Center for Biomedical Research Excellence in the Molecular Basis of Human DiseaseP20GM103486 · NIGMS · UNIVERSITY OF KENTUCKY · PI LOUIS HERSH, LOUIS HERSH LOUIS HERSH · 2012 to 2013
$4.2M
Regulation of Neuronal Survival by the Rit GTPaseR01NS045103 · NINDS · UNIVERSITY OF KENTUCKY · PI ANDRES, DOUGLAS ALLEN · 2003 to 2012
$2.7M
Regulation of Neuronal Survival by the Rit GTPaseR56NS045103 · NINDS · UNIVERSITY OF KENTUCKY · PI ANDRES, DOUGLAS ALLEN · 2008 to 2008
$366k
NIGMS NIH HHS P20 GM103486NINDS NIH HHS NS045103NINDS NIH HHS R01 NS045103NINDS NIH HHS R56 NS045103
6 · The paper itself

Abstract

Rit, a member of the Ras family of GTPases, has been shown to promote cell survival in response to oxidative stress, in part by directing an evolutionarily conserved p38 MAPK-Akt survival cascade. Aberrant Rit signaling has recently been implicated as a driver mutation in human cancer, adding importance to the characterization of critical Rit effector pathways. However, the mechanism by which Rit-p38 signaling regulated Akt activity was unknown. Here, we identify mTORC2 as a critical downstream mediator of Rit-dependent survival signaling in response to reactive oxygen species (ROS) stress. Rit interacts with Sin1 (MAPKAP1), and Rit loss compromises ROS-dependent mTORC2 complex activation, blunting mTORC2-mediated phosphorylation of Akt kinase. Taken together, our findings demonstrate that the p38/mTORC2/Akt signaling cascade mediates Rit-dependent oxidative stress survival. Inhibition of this previously unrecognized cascade should be explored as a potential therapy of Rit-dependent malignancies.

Indexed as

Oxidative StressAdaptor Proteins, Signal TransducingAnimalsApoptosisBlotting, WesternCell ProliferationCells, CulturedEmbryo, MammalianFibroblastsHeLa CellsHumansImmunoprecipitationMechanistic Target of Rapamycin Complex 2MiceMultiprotein Complexesp38 Mitogen-Activated Protein KinasesAdaptor Proteins, Signal TransducingMAPKAP1 protein, humanMechanistic Target of Rapamycin Complex 2Multiprotein Complexesp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktras ProteinsReactive Oxygen SpeciesRIT1 protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID25531880
PMCPMC4274107
OpenAlexW2069873009

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.