Please use this identifier to cite or link to this item: http://hdl.handle.net/10201/48672

Title: Akt1 and Akt2: Differentiating the aktion
Issue Date: 2011
Publisher: Murcia: F. Hernández
ISSN: 1699-5848
0213-3911
Related subjects: 61 - Medicina
Keywords: Akt isoforms
Proliferation
Cancer
Abstract: Kinases of the Akt family are integral and essential components in growth factor signaling pathways activated downstream of the membrane bound phospho-inositol-3 kinase. In light of strong homologies in the primary amino acid sequence, the three Akt kinases were long surmised to play redundant and overlapping roles in insulin signaling across the spectra of cell and tissue types. Over the last 10 years, work using mouse knockout models, cell specific inactivation, and more recently targeted gene inactivation, has brought into question the redundancy within Akt kinase isoforms and instead pointed to isoform specific functions in different cellular events and diseases. Here we concentrate on the differential roles played by Akt1 and Akt2 in a variety of cellular processes and in particular during cancer biogenesis. In this overview, we illustrate that while Akt1 and 2 are often implicated in many aspects of cellular transformation, the two isoforms frequently act in a complementary opposing manner. Furthermore, Akt1 and Akt2 kinases interact differentially with modulating proteins and are necessary in relaying roles during the evolution of cancers from deregulated growth into malignant metastatic killers. These different actions of the two isoforms point to the importance of treatments targeting isoform specific events in the development of effective approaches involving Akt kinases in human disease.
Primary author: Heron-Milhavet, Lisa
Khouya, Nabil
Fernandez, Anne
Lamb, Ned J.
Published in: Histology and Histopathology, vol.26, nº5, 2011
URI: http://hdl.handle.net/10201/48672
Document type: info:eu-repo/semantics/article
Number of pages / Extensions: 12
Rights: info:eu-repo/semantics/openAccess
Temporary material: 1990-2010
Appears in Collections:Vol.26, nº5 (2011)

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