Evidence map›Paper›PMID 11486017›Full record

ArticleMolecular and cellular biology2001

Parallel and independent regulation of interleukin-3 mRNA turnover by phosphatidylinositol 3-kinase and p38 mitogen-activated protein kinase.

X F Ming, G Stoecklin, M Lu, R Looser, C Moroni

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

78 citing papers in PubMed, 173 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Regulation of Postoperative Ileus by Lentivirus-Mediated HuR RNA Interference via the p38/MK2 Signaling Pathway.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2017
    Article
  9. Idelalisib Impacts Cell Growth through Inhibiting Translation-Regulatory Mechanisms in Mantle Cell Lymphoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Article
  10. Article
  11. Review
  12. Article
  13. Coordinated post-transcriptional regulation of the chemokine system: messages from CCL2.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Mechanistic aspects of COX-2 expression in colorectal neoplasia.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2013
    Review
  19. Article
  20. Review

18 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

5 authors at 1 institution in 1 country.

X F MingInstitute for Medical Microbiology, University of Basel, Basel, Switzerland.
G Stoecklin
M Lu
R Looser
C Moroni
University of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

AU-rich elements (ARE) present in the 3' untranslated regions of many cytokines and immediate-early genes are responsible for targeting the transcripts for rapid decay. We present evidence from cotransfection experiments in NIH 3T3 cells that two signaling pathways, one involving phosphatidylinositol 3-kinase (PI3-K), and one involving the p38 mitogen-activated protein kinase (MAPK), lead to stabilization of interleukin-3 mRNA in parallel. Stabilization mediated by either of the two pathways was antagonized by tristetraprolin (TTP), an AU-binding protein known to promote constitutive decay of ARE-containing transcripts. Remarkably, the stabilizing AU-binding protein HuR, in collaboration with p38 MAPK but not with PI3-K, could overcome the destabilizing effect of TTP. These data argue that the stabilizing kinases PI3-K and p38 MAPK do not act through direct inactivation of TTP but via activating pathway-specific stabilizing AU-binding proteins. Our data suggest an integrated model of mRNA turnover control, where stabilizing (HuR) and destabilizing (TTP) AU-binding proteins compete and where the former are under the positive control of independent phosphokinase signaling pathways.

Indexed as

Antigens, SurfaceDNA-Binding ProteinsGene Expression RegulationRNA, MessengerSignal Transduction3T3 CellsAnimalsELAV-Like Protein 1ELAV ProteinsImmediate-Early ProteinsInterleukin-3MiceMitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesRNA-Binding ProteinsAntigens, SurfaceDNA-Binding ProteinsELAVL1 protein, humanELAV-Like Protein 1ELAV ProteinsImmediate-Early ProteinsInterleukin-3Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesRNA-Binding ProteinsRNA, MessengerTristetraprolinZfp36 protein, mouse

Identifiers

PMID11486017
PMCPMC87297
OpenAlexW2152087455

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.