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| MSH2-/- mice are viable but develop lymphoid tumours  | |
mouse Msh2-deficient cells have lost mismatch binding and have acquired microsatellite instability, a mutator phenotype, and tolerance to methylating agents. A significant fraction of Msh2-deficient mice develop lymphomas at an early age |
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MSH2-/- mice develop lymphoblastic lymphomas in association with aberrant expression of rhombotin-2 and Tal-1 |
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ES cells from Msh2(+/-) and Msh2(-/-) mice accumulate oxidized bases as a consequence of low-level radiation exposure |
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absence of Msh2 in Hdh(Q111) mice is sufficient to abrogate progressive Huntington's disease CAG repeat expansion in striatum, eliminate striatal mutant huntingtin with somatically expanded glutamine tracts and to cause an approximately 5 month delay in nuclear mutant protein accumulation |
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MSH2 depletion caused cellular phenotypes associated with defective Fanconi Anemia pathway, including mitomycin C hypersensitivity and chromosomal instability |
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Msh2-null mice were also impaired in locomotive activity and had an abnormal response to heat |