Sotillo, R., Hernando, E., Díaz-Rodríguez, E., Teruya-Feldstein, J., Cordón-Cardo, C., Lowe, S. W., Benezra, R. (January 2007) Mad2 overexpression promotes aneuploidy and tumorigenesis in mice. Cancer Cell, 11 (1). pp. 9-23. ISSN 1535-6108
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Abstract
Mad2 is an essential component of the spindle checkpoint that blocks activation of Separase and dissolution of sister chromatids until microtubule attachment to kinetochores is complete. We show here that overexpression of Mad2 in transgenic mice leads to a wide variety of neoplasias, appearance of broken chromosomes, anaphase bridges, and whole-chromosome gains and losses, as well as acceleration of myc-induced lymphomagenesis. Moreover, continued overexpression of Mad2 is not required for tumor maintenance, unlike the majority of oncogenes studied to date. These results demonstrate that transient Mad2 overexpression and chromosome instability can be an important stimulus in the initiation and progression of different cancer subtypes.
| Item Type: | Paper |
|---|---|
| Uncontrolled Keywords: | APC-DEPENDENT PROTEOLYSIS CHECKPOINT PROTEIN MAD2 MITOTIC CHECKPOINT GENE-EXPRESSION TRANSGENIC MICE CYCLIN-B CHROMOSOME MISSEGREGATION GENOMIC INSTABILITY ANAPHASE INITIATION SPINDLE CHECKPOINT |
| Subjects: | diseases & disorders > cancer bioinformatics > genomics and proteomics > genetics & nucleic acid processing > protein structure, function, modification > protein types > Mad2 organism description > animal > mammal > rodent > mouse bioinformatics > genomics and proteomics > genetics & nucleic acid processing > transgenic animal |
| CSHL Authors: | |
| Communities: | CSHL labs > Lowe lab |
| Depositing User: | CSHL Librarian |
| Date: | January 2007 |
| Date Deposited: | 02 Nov 2011 16:43 |
| Last Modified: | 10 Apr 2018 16:44 |
| PMCID: | PMC1850996 |
| Related URLs: | |
| URI: | https://repository.cshl.edu/id/eprint/23143 |
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