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


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2007-12

AUTHORS

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

ABSTRACT

BACKGROUND: 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 beta-catenin mRNA through an impairment of KSRP function. RESULTS: 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 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. CONCLUSION: 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. More... »

PAGES

28

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1471-2199-8-28

DOI

http://dx.doi.org/10.1186/1471-2199-8-28

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1027768228

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17437629


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