Evidence map›Paper›PMID 22674407›Full record

ArticleJournal of cellular physiology2013

HuR inhibits apoptosis by amplifying Akt signaling through a positive feedback loop.

Mamata Singh, Alaina R Martinez, Suman Govindaraju, Beth S Lee

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Dysregulation of TTP and HuR plays an important role in cancers.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  9. Article
  10. Article
  11. AMPK/HuR-Driven IL-20 Post-Transcriptional Regulation in Psoriatic Skin.The Journal of investigative dermatology · 2015
    Article
  12. Krüppel -like factor 8 is a stress-responsive transcription factor that regulates expression of HuR.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2014
    Article
  13. Review
  14. 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.

Mamata SinghDepartment of Physiology and Cell Biology, The Ohio State University College of Medicine, Columbus, Ohio, USA.
Alaina R Martinez
Suman Govindaraju
Beth S Lee
The Ohio State University · US

Funding

TRANSCRIPTIONAL CONTROL OF VACUOLAR H+-ATPASE EXPRESSIONR01DK052131 · NIDDK · WASHINGTON UNIVERSITY · PI LEE, BETH S. · 1997 to 2009
$2.7M
NIDDK NIH HHS R01 DK052131NIDDK NIH HHS R01 DK052131-14S1
6 · The paper itself

Abstract

Human antigen R (HuR) is a post-transcriptional regulator of gene expression that plays a key role in stabilizing mRNAs during cellular stress, leading to enhanced survival. HuR expression is tightly regulated through multiple transcription and post-transcriptional controls. Although HuR is known to stabilize a subset of mRNAs involved in cell survival, its role in the survival pathway of PI3-kinase/Akt signaling is unclear. Here, we show that in renal proximal tubule cells, HuR performs a central role in cell survival by amplifying Akt signaling in a positive feedback loop. Key to this feedback loop is HuR-mediated stabilization of mRNA encoding Grb10, an adaptor protein whose expression is critical for Akt activation. Stimulation of Akt by interaction with Grb10 then activates NF-κB, which further enhances HuR mRNA and protein expression. This feedback loop is active in unstressed cells, but its effects are increased during stress. Therefore, this study demonstrates a central role for HuR in Akt signaling and reveals a mechanism by which modest changes in HuR levels below or above normal may be amplified, potentially resulting in cell death or cellular transformation.

Indexed as

AnimalsApoptosisCell LineELAV ProteinsFeedback, PhysiologicalGene Expression RegulationGRB10 Adaptor ProteinHumansKidney Tubules, ProximalNF-kappa BPhosphatidylinositol 3-KinasesPolymerase Chain ReactionProtein Array AnalysisProto-Oncogene Proteins c-aktRNA InterferenceRNA, MessengerELAV ProteinsGRB10 Adaptor ProteinGRB10 protein, humanNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Messenger

Identifiers

PMID22674407
PMCPMC3443509
OpenAlexW1989847489

What OpenQuestion holds

Textmetadata
LicenceTDM
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.