Evidence map›Paper›PMID 21444726›Full record

ArticleMolecular and cellular biology2011

A rit GTPase-p38 mitogen-activated protein kinase survival pathway confers resistance to cellular stress.

Geng-Xian Shi, Ling Jin, Douglas A Andres

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  5. The blended phenotype of a germlineCold Spring Harbor molecular case studies · 2021
    Article
  6. Review
  7. Article
  8. Review
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  10. Article
  11. Elevated expression of RIT1 correlates with poor prognosis in endometrial cancer.International journal of clinical and experimental pathology · 2015
    Article
  12. Article
  13. Review
  14. Article
  15. Article
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  19. Article
  20. Rit GTPase signaling promotes immature hippocampal neuronal survival.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    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.

Geng-Xian ShiDepartment of Molecular and Cellular Biochemistry, University of Kentucky College of Medicine, Lexington, KY 40536-0509, USA.
Ling Jin
Douglas A Andres
University of Kentucky · US

Funding

UNDERSTANDING THE MOLECULAR BASIS OF EPIGENETIC TRANSCRIPTIONAL SILENCINGP20RR020171 · NCRR · UNIVERSITY OF KENTUCKY · PI LOUIS HERSH, LOUIS HERSH LOUIS HERSH · 2004 to 2011
$16.5M
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
NCRR NIH HHS 2P20 RR020171NCRR NIH HHS P20 RR020171NINDS NIH HHS NS045103NINDS NIH HHS R01 NS045103NINDS NIH HHS R56 NS045103
6 · The paper itself

Abstract

Cells mobilize diverse signaling cascades to protect against stress-mediated injury. Ras family GTPases play a pivotal role in cell fate determination, serving as molecular switches to control the integration of multiple signaling pathways. p38 mitogen-activated protein kinase (MAPK) signaling serves as a critical fulcrum in this process, regulating networks that stimulate cellular apoptosis but also have the capacity to promote cell survival. However, relatively little is known concerning this functional dichotomy, particularly the regulation of p38-dependent survival pathways. Here, we demonstrate that the Rit GTPase promotes cell survival by directing an unexpected p38 MAPK-dependent AKT survival pathway. Following stress exposure, Rit small hairpin RNA interference (shRNAi)-treated cells display increased apoptosis and selective disruption of p38 MAPK signaling, while expression of constitutively activated Rit promotes p38-AKT-dependent cell survival. Rit, but not Ras or Rap GTPases, can associate with, and is critical for, stress-mediated activation of the scaffolded p38-MK2-HSP27-AKT prosurvival signaling complex. Together, our studies establish Rit as a central regulator of a p38 MAPK-dependent signaling cascade that functions as a critical cellular survival mechanism in response to stress.

Indexed as

MAP Kinase Signaling SystemStress, PhysiologicalAnimalsApoptosisCell Line, TumorCell SurvivalHeLa CellsHSP27 Heat-Shock ProteinsHumansp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktras ProteinsRatsRNA InterferenceRNA, Small InterferingSignal TransductionHSP27 Heat-Shock Proteinsp38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktras ProteinsRIT1 protein, humanRNA, Small Interfering

Identifiers

PMID21444726
PMCPMC3133351
OpenAlexW2121295484

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.