Cellular Werner Phenotypes in Mice Expressing a Putative Dominant-Negative Human WRN Gene | Zendy

Lan Wang | Zendy; Charles E. Ogburn | Zendy; Carol B. Ware | Zendy; Warren Ladiges | Zendy; Hagop Youssoufian | Zendy; George M. Martin | Zendy; Junko Oshima | Zendy

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Cellular Werner Phenotypes in Mice Expressing a Putative Dominant-Negative Human WRN Gene

Author(s) -

Lan Wang,

Charles E. Ogburn,

Carol B. Ware,

Warren Ladiges,

Hagop Youssoufian,

George M. Martin,

Junko Oshima

Publication year - 2000

Publication title -

genetics

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.792

H-Index - 246

eISSN - 1943-2631

pISSN - 0016-6731

DOI - 10.1093/genetics/154.1.357

Subject(s) - werner syndrome , biology , genetics , phenotype , locus (genetics) , gene , genetically modified mouse , premature aging , helicase , transgene , microbiology and biotechnology , endogeny , mutation , rna , endocrinology

Mutations at the Werner helicase locus (WRN) are responsible for the Werner syndrome (WS). WS patients prematurely develop an aged appearance and various age-related disorders. We have generated transgenic mice expressing human WRN with a putative dominant-negative mutation (K577M-WRN). Primary tail fibroblast cultures from K577M-WRN mice showed three characteristics of WS cells: hypersensitivity to 4-nitroquinoline-1-oxide (4NQO), reduced replicative potential, and reduced expression of the endogenous WRN protein. These data suggest that K577M-WRN mice may provide a novel mouse model for the WS.

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