HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Supplemental Data All Versions of this Article: fj.06-7684comv1 21/10/2273    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Noguchi, M. Articles by Suizu, F. Search for Related Content PubMed PubMed Citation Articles by Noguchi, M. Articles by Suizu, F.

Proto-oncogene TCL1: more than just a coactivator for Akt

Masayuki Noguchi^*,1, Virginie Ropars, Christian Roumestand and Futoshi Suizu^*

^* Division of Cancer Biology Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan; and

CNRS, UMR5048, Centre de Biochimie Structurale, F34090 Montpellier, France; INSERM, U554, F34090 Montpellier, France; Universitet Montpellier 1 et 2, F34090 Montpellier, France

¹ Correspondence: N15, W7, Kita-ku, Sapporo 060-0815, Japan. E-mail: m_noguch{at}igm.hokudai.ac.jp

Serine threonine kinase Akt, also called PKB (protein kinase B), plays a central role in regulating intracellular survival. Deregulation of this Akt signaling pathway underlies various human neoplastic diseases. Recently, the proto-oncogene TCL1 (T cell leukemia 1), with a previously unknown physiological function, was shown to interact with the Akt pleckstrin homology domain, enhancing Akt kinase activity; hence, it functions as an Akt kinase coactivator. In contrast to pathological conditions in which the TCL1 gene is highly activated in various human neoplasmic diseases, the physiological expression of TCL1 is tightly limited to early developmental cells as well as various developmental stages of immune cells. The NBRE (nerve growth factor-responsive element) of the proximal TCL1 promoter sequences can regulate the restricted physiological expression of TCL1 in a negative feedback mechanism. Further, based on the NMR structural studies of Akt-TCL1 protein complexes, an inhibitory peptide, "Akt-in," consisting of the ßA strand of TCL1, has been identified and has therapeutic potential. This review article summarizes and discusses recent advances in the understanding of TCL1-Akt functional interaction in order to clarify the biological action of the proto-oncogene TCL1 family and the development avenues for a suppressive drug specific for Akt, a core intracellular survival regulator.—Noguchi, M., Ropars, V., Roumestand, C., Suizu, F. Proto-oncogene TCL1: more than just a coactivator for Akt.

Key Words: protein kinase B • T cell leukemia 1 • Akt-PH domain • isoform

This article has been cited by other articles:

				M. Herling, K. A. Patel, M. A. Teitell, M. Konopleva, F. Ravandi, R. Kobayashi, and D. Jones High TCL1 expression and intact T-cell receptor signaling define a hyperproliferative subset of T-cell prolymphocytic leukemia Blood, January 1, 2008; 111(1): 328 - 337. [Abstract] [Full Text] [PDF]

				G. Despouy, M. Joiner, E. Le Toriellec, R. Weil, and M. H. Stern The TCL1 oncoprotein inhibits activation-induced cell death by impairing PKC{theta} and ERK pathways Blood, December 15, 2007; 110(13): 4406 - 4416. [Abstract] [Full Text] [PDF]

				A. He, L. Zhu, N. Gupta, Y. Chang, and F. Fang Overexpression of Micro Ribonucleic Acid 29, Highly Up-Regulated in Diabetic Rats, Leads to Insulin Resistance in 3T3-L1 Adipocytes Mol. Endocrinol., November 1, 2007; 21(11): 2785 - 2794. [Abstract] [Full Text] [PDF]