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Transgenic mice for cre‐inducible overexpression of the Cul4A gene
Author(s) -
Li Tong,
Hung MingSzu,
Wang Yucheng,
Mao JianHua,
Tan JiaLi,
Jahan Kenneth,
Roos Hannah,
Xu Zhidong,
Jablons David M.,
You Liang
Publication year - 2011
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.20708
Subject(s) - cre recombinase , transgene , biology , genetically modified mouse , conditional gene knockout , gene knockout , gene targeting , microbiology and biotechnology , reporter gene , gene , knockout mouse , transfection , cancer research , gene expression , genetics , phenotype
Abstract The Cullin 4A ( Cul4A ) gene is important in cell survival, development, growth, and cell cycle control and is amplified in breast and hepatocellular cancers. Recently, we reported that Cul4A plays an oncogenic role in the pathogenesis of mesothelioma. An important strategy for studying Cul4A in different tissues is targeted overexpression of this gene in vivo . Studies of Cul4A in mice have been restricted to the loss‐of‐function studies using Cul4A knockout mice; gain‐of‐function studies of Cul4A using transgenic mice have not been reported. We, therefore, generated a gain‐of‐function transgenic mouse model that overexpresses Cul4A in a Cre‐dependent manner. Before Cre recombination, these mice express LacZ during development in most adult tissues. After Cre‐mediated excision of the LacZ reporter, the transfected Cul4A gene is expressed along with a C‐terminal Myc‐tag in different tissues. In this study, Cre‐excision was induced in mouse lungs by inhalation of an adenovirus vector encoding Cre recombinase. This mouse model provides a valuable resource for investigating the significance of Cul4A overexpression in various tissues. genesis 49:134–141, 2011. © 2011 Wiley‐Liss, Inc.