http://www.cnr.it/ontology/cnr/individuo/prodotto/ID287109

Prohibitin 2 represents a novel nuclear AKT substrate during all-trans retinoic acid-induced differentiation of acute promyelocytic leukemia cells (Articolo in rivista)

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Prohibitin 2 represents a novel nuclear AKT substrate during all-trans retinoic acid-induced differentiation of acute promyelocytic leukemia cells (Articolo in rivista) (literal)

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Bavelloni A, Piazzi M, Faenza I, Raffini M, D'Angelo A, Cattini L, Cocco L, Blalock WL (2014)
Prohibitin 2 represents a novel nuclear AKT substrate during all-trans retinoic acid-induced differentiation of acute promyelocytic leukemia cells
in The FASEB journal (Online)
(literal)

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Bavelloni A, Piazzi M, Faenza I, Raffini M, D'Angelo A, Cattini L, Cocco L, Blalock WL (literal)

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Struttura Complessa (SC) Laboratory of Musculoskeletal Cell Biology, Rizzoli Orthopedic Institute, Bologna, Italy; Ramses Laboratory, Rizzoli Orthopedic Institute, Bologna, Italy; Cell Signaling Laboratory, Department of Biomedical Sciences, University of Bologna, Bologna, Italy; National Research Council (CNR) of Italy, Institute of Molecular Genetics (IGM), Rizzoli Orthopedic Institute, via di Barbiano, 1/10, 40136 Bologna, Italy (literal)

Titolo

Prohibitin 2 represents a novel nuclear AKT substrate during all-trans retinoic acid-induced differentiation of acute promyelocytic leukemia cells (literal)

Abstract

The AKT/PKB kinase is essential for cell survival, proliferation, and differentiation; however, aberrant AKT activation leads to the aggressiveness and drug resistance of many human neoplasias.In the human acute promyelocytic leukemia cell line NB4, nuclear AKT activity increases during all-trans retinoic acid (ATRA)-mediated differentiation. As nuclear AKT activity is associated with differentiation, we sought to identify the nuclear substrates of AKT that were phosphorylated after ATRA treatment. A proteomics-based search for nuclear substrates of AKT in ATRA-treated NB4 cells was undertaken by using 2D-electrophoresis/mass spectrometry (MS) in combination with an anti-AKT phospho-substrate antibody. Western blot analysis, an in vitro kinase assay, and/or site-directed mutagenesis were performed to further characterize the MS findings. MS analysis revealed prohibitin (PHB)-2, a multifunctional protein involved in cell cycle progression and the suppression of oxidative stress, to be a putative nuclear substrate of AKT. Follow-up studies confirmed that AKT phosphorylates PHB2 on Ser-91 and that forced expression of the PHB2(S91A) mutant results in a rapid loss of viability and apoptotic cell death. Activation of nuclear AKT during ATRA-mediated differentiation results in the phosphorylation of several proteins, including PHB2, which may serve to coordinate nuclear-mitochondrial events during differentiation. © FASEB. (literal)

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