Open Access Open Badges Research article

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

Tina Ruggiero1, Michele Trabucchi1, Marco Ponassi1, Giorgio Corte12, Ching-Yi Chen3, Latifa al-Haj4, Khalid SA Khabar4, Paola Briata1 and Roberto Gherzi1*

  • * Corresponding author: Roberto Gherzi

  • † Equal contributors

Author Affiliations

1 Istituto Nazionale per la Ricerca sul Cancro (IST), 16132 Genova, Italy

2 DOBIG, University of Genova, 16132 Genova, Italy

3 Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, AL 35294, USA

4 Program in Biomolecular Research, King Faisal Specialist Hospital and Research Center, Riyadh 11211, Saudi Arabia

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BMC Molecular Biology 2007, 8:28  doi:10.1186/1471-2199-8-28

Published: 16 April 2007



KSRP 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 β-catenin mRNA through an impairment of KSRP function.


Aim 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 αT3-1 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 β-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.


Our 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.