Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/107569
Title: Absence of ERK5/MAPK7 delays tumorigenesis in Atm-/- mice
Author: Granados Jaén, Alba
Angulo Ibáñez, María
Rovira Clavé, Xavier
Vasquez Gamez, Celina Paola
Soriano Zaragoza, Francesc X. (Francesc Xavier)
Reina del Pozo, Manuel
Espel Masferrer, Enric
Keywords: Proteïnes quinases
Reparació de l'ADN
Limfomes
Protein kinases
DNA repair
Lymphomas
Issue Date: 25-Oct-2016
Publisher: Impact Journals
Abstract: Ataxia-telangiectasia mutated (ATM) is a cell cycle checkpoint kinase that upon activation by DNA damage leads to cell cycle arrest and DNA repair or apoptosis. The absence of Atm or the occurrence of loss-of-function mutations in Atm predisposes to tumorigenesis. MAPK7 has been implicated in numerous types of cancer with pro-survival and pro-growth roles in tumor cells, but its functional relation with tumor suppressors is not clear. In this study, we show that absence of MAPK7 delays death due to spontaneous tumor development in Atm-/- mice. Compared with Atm-/- thymocytes, Mapk7-/-Atm-/- thymocytes exhibited an improved response to DNA damage (increased phosphorylation of H2AX) and a restored apoptotic response after treatment of mice with ionizing radiation. These findings define an antagonistic function of ATM and MAPK7 in the thymocyte response to DNA damage, and suggest that the lack of MAPK7 inhibits thymic lymphoma growth in Atm-/- mice by partially restoring the DNA damage response in thymocytes.
Note: Reproducció del document publicat a: http://doi.org/10.18632/oncotarget.12908
It is part of: Oncotarget, 2016, vol. 7, num. 46, p. 74435-74447
URI: http://hdl.handle.net/2445/107569
Related resource: http://doi.org/10.18632/oncotarget.12908
ISSN: 1949-2553
Appears in Collections:Articles publicats en revistes (Biologia Cel·lular, Fisiologia i Immunologia)

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