Evidence map›Paper›PMID 24069528›Full record

ArticleeLife2013

Cavin-3 dictates the balance between ERK and Akt signaling.

Victor J Hernandez, Jian Weng, Peter Ly, Shanica Pompey, Hongyun Dong, Lopa Mishra, Margaret Schwarz, Richard G W Anderson, Peter Michaely

Open access · goldAbstract read
In one paragraph

Article in eLife, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
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  4. Review
  5. Review
  6. Neonatal lethality of mouse A/J-7Mammalian genome : official journal of the International Mammalian Genome Society · 2023
    Article
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  13. Assessment ofCell journal · 2021
    Article
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  15. Article
  16. Article
  17. Article
  18. Review
  19. A Role for Caveolin-3 in the Pathogenesis of Muscular Dystrophies.International journal of molecular sciences · 2020
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Victor J HernandezDepartment of Cell Biology , University of Texas Southwestern Medical Center , Dallas , United States.
Jian Weng
Peter Ly
Shanica Pompey
Hongyun Dong
Lopa Mishra
Margaret Schwarz
Richard G W Anderson
Peter Michaely
The University of Texas Southwestern Medical Center · USThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Cell Biology Research Improvements and RenovationsC06RR030414 · NCRR · UT SOUTHWESTERN MEDICAL CENTER · PI FITZ, JOHN GREGORY · 2010 to 2010
$15.0M
Targeting CDK4 in TGS-B Inactivated Gastrointestinal CancersP01CA130821 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MISHRA, LOPA · 2008 to 2013
$6.9M
FUNCTION OF CAVEOLAE IN POTOCYTOSIS AND CELL SIGNALINGR01GM052016 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI MICHAELY, PETER A. · 1995 to 2010
$4.9M
Role of Beta Spectrin and Smad in Alcohol-Induced Liver and GI Cell ProliferationR01AA023146 · NIAAA · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Lopa Mishra · 2013 to 2026
$4.6M
Characterization of the Role of ARH on LDLR FunctionR01HL085218 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI MICHAELY, PETER A. · 2006 to 2015
$2.3M
EMAP II: Pulmonary Vascular MediatorR01HL114977 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI SCHWARZ, MARGARET A · 2012 to 2015
$1.8M
NCI NIH HHS CA130821NCI NIH HHS P01 CA130821NCI NIH HHS P30 CA016672NCRR NIH HHS C06 RR030414NHLBI NIH HHS HL085218NHLBI NIH HHS R01 HL085218NHLBI NIH HHS R01 HL114977NIGMS NIH HHS GM052016NIGMS NIH HHS R01 GM052016
6 · The paper itself

Abstract

Cavin-3 is a tumor suppressor protein of unknown function. Using both in vivo and in vitro approaches, we show that cavin-3 dictates the balance between ERK and Akt signaling. Loss of cavin-3 increases Akt signaling at the expense of ERK, while gain of cavin-3 increases ERK signaling at the expense Akt. Cavin-3 facilitates signal transduction to ERK by anchoring caveolae to the membrane skeleton of the plasma membrane via myosin-1c. Caveolae are lipid raft specializations that contain an ERK activation module and loss of the cavin-3 linkage reduces the abundance of caveolae, thereby separating this ERK activation module from signaling receptors. Loss of cavin-3 promotes Akt signaling through suppression of EGR1 and PTEN. The in vitro consequences of the loss of cavin-3 include induction of Warburg metabolism (aerobic glycolysis), accelerated cell proliferation, and resistance to apoptosis. The in vivo consequences of cavin-3 knockout are increased lactate production and cachexia. DOI:http://dx.doi.org/10.7554/eLife.00905.001.

Indexed as

ApoptosisCell LineEnzyme ActivationExtracellular Signal-Regulated MAP KinasesHumansIntracellular Signaling Peptides and ProteinsProto-Oncogene Proteins c-aktSignal TransductionCAVIN3 protein, humanExtracellular Signal-Regulated MAP KinasesIntracellular Signaling Peptides and ProteinsProto-Oncogene Proteins c-aktaerobic glycolysisAktCavin-3ERKhSRBCHumanMousePRKCDBP

Identifiers

PMID24069528
PMCPMC3780650
OpenAlexW2118006087

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.