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 Blood, 25 June 2009, Vol. 113, No. 26, pp. 6695-6698.
Prepublished online as a Blood First Edition Paper on April 30, 2009; DOI 10.1182/blood-2008-07-166835.

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LYMPHOID NEOPLASIA

Brief report

TGF-β induces degradation of TAL1/SCL by the ubiquitin-proteasome pathway through AKT-mediated phosphorylation

Jean-Michel Terme1, Ludovic Lhermitte2, Vahid Asnafi2, and Pierre Jalinot1

1 Laboratoire de Biologie Moléculaire de la Cellule, Unité Mixte de Recherche (UMR) 5239, Centre National de la Recherche Scientifique (CNRS), École Normale Supérieure de Lyon, Institut Fédératif de Recherche 128 Biosciences Lyon Gerland, Lyon; and 2 Université Paris 5 Descartes, UMR 8147, CNRS, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Necker-Enfants-Malades, Hematology Department, Paris, France

T-cell acute lymphoblastic leukemia 1 (TAL1), also known as stem cell leukemia (SCL), plays important roles in differentiation of hematopoietic and endothelial cells and is deregulated in a high percentage of T-cell acute lymphoblastic leukemia (T-ALL). In this report we show that the intracellular concentration of TAL1 is regulated by transforming growth factor β (TGF-β), which triggers its polyubiquitylation and degradation by the proteasome. This effect is mediated by AKT1, which phosphorylates TAL1 at threonine 90. Immunoprecipitation experiments showed that this event increases association of TAL1 with the E3 ubiquitin ligase CHIP. The E47 heterodimerization partner of TAL1 hinders this association. Our observations indicate that activation of the TGF-β and phosphatidylinositol 3-kinase/AKT pathways might reverse overexpression of TAL1 in leukemic cells by inducing proteolysis of this important oncogene.


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