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The putative tumor suppressor gene EphA7 is a novel BMI-1 target

Bmi1 was originally identified as a gene that contributes to the development of mouse lymphoma by inhibiting MYC-induced apoptosis through repression of Ink4a and Arf. It codes for the Polycomb group protein BMI-1 and acts primarily as a transcriptional repressor via chromatin modifications. Althoug...

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Detalles Bibliográficos
Autores principales: Prost, Gaëlle, Braun, Sebastian, Hertwig, Falk, Winkler, Marcus, Jagemann, Lucas, Nolbrant, Sara, Leefa, Isabelle V., Offen, Nils, Miharada, Kenichi, Lang, Stefan, Artner, Isabella, Nuber, Ulrike A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295425/
https://www.ncbi.nlm.nih.gov/pubmed/27533460
http://dx.doi.org/10.18632/oncotarget.11279
Descripción
Sumario:Bmi1 was originally identified as a gene that contributes to the development of mouse lymphoma by inhibiting MYC-induced apoptosis through repression of Ink4a and Arf. It codes for the Polycomb group protein BMI-1 and acts primarily as a transcriptional repressor via chromatin modifications. Although it binds to a large number of genomic regions, the direct BMI-1 target genes described so far do not explain the full spectrum of BMI-1-mediated effects. Here we identify the putative tumor suppressor gene EphA7 as a novel direct BMI-1 target in neural cells and lymphocytes. EphA7 silencing has been reported in several different human tumor types including lymphomas, and our data suggest BMI1 overexpression as a novel mechanism leading to EphA7 inactivation via H3K27 trimethylation and DNA methylation.