Evidence map›Paper›PMID 20018854›Full record

ArticleThe Journal of biological chemistry2010

Transcriptional control of human antigen R by bone morphogenetic protein.

Selvi C Jeyaraj, Mamata Singh, Dina A Ayupova, Suman Govindaraju, Beth S Lee

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Human antigen R and drug resistance in tumors.Investigational new drugs · 2019
    Review
  8. Article
  9. Article
  10. 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
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. The RNA-binding protein human antigen R controls global changes in gene expression during Schwann cell development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  17. HuR function in disease.Frontiers in bioscience (Landmark edition) · 2012
    Review
  18. 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

5 authors at 2 institutions in 1 country.

Selvi C JeyarajDepartment of Physiology and Cell Biology, The Ohio State University College of Medicine, Columbus, Ohio 43210, USA.
Mamata Singh
Dina A Ayupova
Suman Govindaraju
Beth S Lee
The Ohio State University · USRadiation Oncology Associates · US

Funding

TRANSCRIPTIONAL CONTROL OF VACUOLAR H+-ATPASE EXPRESSIONR01DK052131 · NIDDK · WASHINGTON UNIVERSITY · PI LEE, BETH S. · 1997 to 2009
$2.7M
DYNAMICS OF THE ACTIN CYTOSKELETON IN OSTEOCLASTSR01AR051515 · NIAMS · OHIO STATE UNIVERSITY · PI LEE, BETH S. · 2006 to 2009
$1.0M
NIAMS NIH HHS R01 AR051515NIDDK NIH HHS R01 DK052131
6 · The paper itself

Abstract

Human antigen R (HuR) is an RNA-binding protein with protective activities against cellular stress. This study considers the mechanisms by which HuR transcriptional regulation occurs in renal proximal tubule cells. Under basal conditions, HuR mRNA is expressed in two forms: one that contains a approximately 20-base 5'-untranslated region (UTR) sequence and one that contains a approximately 150-base, G+C-rich 5'-UTR that is inhibitory to translation. Recovery from cellular stresses such as thapsigargin and ATP depletion induced increased expression of the shorter, more translatable transcript and decreased expression of the longer form. Analysis of HuR upstream regions revealed sequences necessary for regulation of the shorter mRNA. Within the long, G+C-rich 5'-UTR exist multiple copies of the alternate Smad 1/5/8-binding motif GCCGnCGC. Recovery from ATP depletion induced increases in Smad 1/5/8 levels; further, gel shift and chromatin immunoprecipitation analyses demonstrated the ability of these Smads to bind to the relevant motif in the HuR 5'-UTR. Transfection of exogenous Smad 1 increased HuR mRNA expression. Finally, HuR mRNA expression driven by the Smad-binding sites was responsive to BMP-7, a protein with known protective effects against ischemic injury in kidney. These data suggest that transcriptional induction of a readily translatable HuR mRNA may be driven by a mechanism known to protect the kidney from injury and provides a novel pathway through which administration of BMP-7 may attenuate renal damage.

Indexed as

5' Untranslated RegionsAdenosine TriphosphateAnimalsAntigens, SurfaceBase CompositionBlotting, WesternBone Morphogenetic Protein 7Cell LineChromatin ImmunoprecipitationELAV-Like Protein 1ELAV ProteinsElectrophoretic Mobility Shift AssayEnzyme-Linked Immunosorbent AssayImmunohistochemistryPromoter Regions, GeneticProtein Binding5' Untranslated RegionsAdenosine TriphosphateAntigens, SurfaceBone Morphogenetic Protein 7ELAVL1 protein, humanELAV-Like Protein 1ELAV ProteinsRNA-Binding ProteinsSmad1 ProteinSmad5 ProteinSmad8 Protein

Identifiers

PMID20018854
PMCPMC2836048
OpenAlexW2007011637

What OpenQuestion holds

Textmetadata
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.