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IWANAGA, Yoichi; CHI, Ya-Hui; MIYAZATO, Akiko; SHELEG, Sergey; HALLER, Kerstin; PELOPONESE, Jean-Marie; YAN LI; WARD, Jerrold M; BENEZRA, Robert; JEANG, Kuan-Teh
Cancer research (Chicago, Ill.), 01/2007, Letnik: 67, Številka: 1Journal Article
Mitotic arrest-deficient protein 1 (MAD1) is a component of the mitotic spindle assembly checkpoint. We have created a knockout mouse model to examine the physiologic consequence of reduced MAD1 function. Mad1(+/-) mice were successfully generated, but repeated paired mating of Mad1(+/-) with Mad1(+/-) mice failed to produce a single Mad1(-/-) animal, suggesting that the latter genotype is embryonic lethal. In aging studies conducted for >18 months, Mad1(+/-) mice compared with control wild-type (wt) littermates showed a 2-fold higher incidence of constitutive tumors. Moreover, 42% of Mad1(+/-) (P < 0.03), but 0% of wt, mice developed neoplasia after treatment with vincristine, a microtubule depolymerization agent. Mad1(+/-) mouse embryonic fibroblasts (MEF) were found to be more prone than wt cells to become aneuploid; Mad1(+/-), but not wt, MEFs produced fibrosarcomas when explanted into nude mice. Our results indicate an essential MAD1 function in mouse development and correlate Mad1 haploinsufficiency with increased constitutive tumors.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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