Evidence map›Paper›PMID 17437629›Full record

ArticleBMC molecular biology2007

Identification of a set of KSRP target transcripts upregulated by PI3K-AKT signaling.

Tina Ruggiero, Michele Trabucchi, Marco Ponassi, Giorgio Corte, Ching-Yi Chen, Latifa al-Haj, Khalid S A Khabar, Paola Briata, Roberto Gherzi

Open access · hybridAbstract read
In one paragraph

Article in BMC molecular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Expanding the Functions of KHSRP Protein: Insights into DNA G-Quadruplex Binding.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  3. Article
  4. Aging and Protein Kinases.Advances in experimental medicine and biology · 2021
    Article
  5. Review
  6. Review
  7. Article
  8. Hallmarks of cancer and AU-rich elements.Wiley interdisciplinary reviews. RNA · 2017
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. H19 long noncoding RNA controls the mRNA decay promoting function of KSRP.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  14. Article
  15. Role of KSRP in control of type I interferon and cytokine expression.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

9 authors at 3 institutions in 3 countries.

Tina RuggieroIstituto Nazionale per la Ricerca sul Cancro (IST), 16132 Genova, Italy. tina.ruggiero@istge.it <tina.ruggiero@istge.it>
Michele Trabucchi
Marco Ponassi
Giorgio Corte
Ching-Yi Chen
Latifa al-Haj
Khalid S A Khabar
Paola Briata
Roberto Gherzi
Alleanza Contro il Cancro · ITKing Faisal Specialist Hospital & Research Centre · SAUniversity of Alabama at Birmingham · US

Funding

Telethon GGP04012
6 · The paper itself

Abstract

backgroundKSRP is a AU-rich element (ARE) binding protein that causes decay of select sets of transcripts in different cell types. We have recently described that phosphatidylinositol 3-kinase/AKT (PI3K-AKT) activation induces stabilization and accumulation of the labile beta-catenin mRNA through an impairment of KSRP function.

resultsAim of this study was to identify additional KSRP targets whose stability and steady-state levels are enhanced by PI3K-AKT activation. First, through microarray analyses of the AU-rich transcriptome in pituitary alphaT3-1 cells, we identified 34 ARE-containing transcripts upregulated in cells expressing a constitutively active form of AKT1. In parallel, by an affinity chromatography-based technique followed by microarray analyses, 12 mRNAs target of KSRP, additional to beta-catenin, were identified. Among them, seven mRNAs were upregulated in cells expressing activated AKT1. Both steady-state levels and stability of these new KSRP targets were consistently increased by either KSRP knock-down or PI3K-AKT activation.

conclusionOur study identified a set of transcripts that are targets of KSRP and whose expression is increased by PI3K-AKT activation. These mRNAs encode RNA binding proteins, signaling molecules and a replication-independent histone. The increased expression of these gene products upon PI3K-AKT activation could play a role in the cellular events initiated by this signaling pathway.

Indexed as

Gene Expression ProfilingAnimalsCells, CulturedHeterogeneous Nuclear Ribonucleoprotein A1Heterogeneous-Nuclear Ribonucleoprotein DHeterogeneous Nuclear Ribonucleoprotein D0Heterogeneous-Nuclear Ribonucleoprotein Group A-BMiceOligonucleotide Array Sequence AnalysisPhosphatidylinositol 3-KinasesProtein BindingProto-Oncogene Proteins c-aktRatsRecombinant ProteinsRNA-Binding ProteinsRNA, MessengerHeterogeneous Nuclear Ribonucleoprotein A1Heterogeneous-Nuclear Ribonucleoprotein DHeterogeneous Nuclear Ribonucleoprotein D0Heterogeneous-Nuclear Ribonucleoprotein Group A-BHnrnpd protein, ratHnrpd protein, mouseKhsrp protein, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRecombinant ProteinsRNA-Binding ProteinsRNA, MessengerTrans-Activators

Identifiers

PMID17437629
PMCPMC1858702
OpenAlexW2074230342

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.