Evidence map›Paper›PMID 19884656›Full record

ArticleThe Journal of clinical investigation2009

Essential role of the RNA-binding protein HuR in progenitor cell survival in mice.

Mallika Ghosh, Hector Leonardo Aguila, Jason Michaud, Youxi Ai, Ming-Tao Wu, Annabrita Hemmes, Ari Ristimaki, Caiying Guo, Henry Furneaux, Timothy Hla

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

137 citing papers in PubMed, 199 citations in OpenAlex.

  1. Article
  2. Article
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  4. Endothelial Elavl1 Is Required for CD8 T-Cell Persistence in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. CRL2BMC biology · 2025
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Elavl1 is dispensable for appendicular skeletal development.bioRxiv : the preprint server for biology · 2024
    Article
  18. Article
  19. Article
  20. Article

77 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 2 countries.

Mallika GhoshCenter for Vascular Biology, University of Connecticut Health Center, Farmington, Connecticut, USA.
Hector Leonardo Aguila
Jason Michaud
Youxi Ai
Ming-Tao Wu
Annabrita Hemmes
Ari Ristimaki
Caiying Guo
Henry Furneaux
Timothy Hla
Center for Vascular Biology Research · USUConn Health · USHelsinki University Hospital · FIUniversity of Helsinki · FI

Funding

THE ROLE OF ENDOCANNABINOIDS AND THEIR RECEPTORS IN COLORECTAL CANCERP01CA077839 · NCI · VANDERBILT UNIVERSITY · PI DUBOIS, RAYMOND N. · 1999 to 2016
$17.8M
Post-Transcriptional Mechanisms and Vascular InflammationR01HL049094 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI HLA, TIMOTHY TUN · 1993 to 2013
$4.2M
NCI NIH HHS CA-77839NCI NIH HHS P01 CA077839NHLBI NIH HHS HL49094NHLBI NIH HHS R01 HL049094
6 · The paper itself

Abstract

The RNA-binding protein HuR (also known as ELAV1) binds to the 3'-untranslated region of mRNAs and regulates transcript stability and translation. However, the in vivo functions of HuR are not well understood. Here, we report that murine HuR is essential for life; postnatal global deletion of Elavl1 induced atrophy of hematopoietic organs, extensive loss of intestinal villi, obstructive enterocolitis, and lethality within 10 days. Upon Elavl1 deletion, progenitor cells in the BM, thymus, and intestine underwent apoptosis, whereas quiescent stem cells and differentiated cells were unaffected. The survival defect of hematopoietic progenitor cells was cell intrinsic, as transplant of Elavl1-/- BM led to compromised hematopoietic reconstitution but did not cause lethality. Expression of p53 and its downstream effectors critical for cell death were induced in progenitor cells as HuR levels declined. In mouse embryonic fibroblasts, HuR bound to and stabilized the mRNA for Mdm2, a critical negative regulator of p53. Furthermore, cell survival was restored by expression of Mdm2 in Elavl1-/- cells, suggesting that HuR keeps p53 levels in check in progenitor cells and thereby promotes cell survival. This regulation of cell stress response by HuR in progenitor cells, which we believe to be novel, could potentially be exploited in cytotoxic anticancer therapies as well as stem cell transplant therapy.

Indexed as

AnimalsAntigens, SurfaceApoptosisCell DifferentiationCell SurvivalELAV-Like Protein 1ELAV ProteinsFemaleGastrointestinal TractGene DeletionHematopoiesisHematopoietic Stem CellsMaleMiceMice, KnockoutModels, BiologicalAntigens, SurfaceELAVL1 protein, humanELAV-Like Protein 1ELAV ProteinsMdm2 protein, mouseProto-Oncogene Proteins c-mdm2RNA-Binding ProteinsRNA, MessengerTamoxifenTumor Suppressor Protein p53

Identifiers

PMID19884656
PMCPMC2786787
OpenAlexW2093422430

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.