SET/I2PP2A overexpression induces phenotypic, molecular, and metabolic alterations in an oral keratinocyte cell line

Author:

Sobral Lays M.12,Coletta Ricardo D.3,Alberici Luciane C.4,Curti Carlos4,Leopoldino Andréia M.12

Affiliation:

1. Department of Clinical Analyses, Toxicology and Food Sciences; School of Pharmaceutical Sciences of Ribeirão Preto; University of São Paulo; SP Brazil

2. CEPID-FAPESP; Center for Cell Based Therapy; School of Medicine of Ribeirão Preto; University of São Paulo; SP Brazil

3. Department of Oral Diagnosis; Piracicaba Dental School; University of Campinas; Piracicaba SP Brazil

4. Department of Physics and Chemistry; School of Pharmaceutical Sciences of Ribeirão Preto; University of São Paulo; SP Brazil

Funder

Fundação de Amparo à Pesquisa do Estado de São Paulo

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior

Conselho Nacional de Desenvolvimento Científico e Tecnológico

Publisher

Wiley

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference43 articles.

1. Identification and characterization of SET, a nuclear phosphoprotein encoded by the translocation break point in acute undifferentiated leukemia;Adachi;J Biol Chem,1994

2. The myeloid leukemia-associated protein SET is a potent inhibitor of protein phosphatase 2A;Li;J Biol Chem,1996

3. Targeting SET/I(2)PP2A oncoprotein functions as a multi-pathway strategy for cancer therapy;Switzer;Oncogene,2011

4. Rac1-induced cell migration requires membrane recruitment of the nuclear oncogene SET;Klooster;EMBO J,2007

5. Cytoplasmic targeting of the proto-oncogene SET promotes cell spreading and migration;Lam;FEBS Lett,2013

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