Mouse development with a single E2F activator

被引:0
|
作者
Shih-Yin Tsai
Rene Opavsky
Nidhi Sharma
Lizhao Wu
Shan Naidu
Eric Nolan
Enrique Feria-Arias
Cynthia Timmers
Jana Opavska
Alain de Bruin
Jean-Leon Chong
Prashant Trikha
Soledad A. Fernandez
Paul Stromberg
Thomas J. Rosol
Gustavo Leone
机构
[1] College of Biological Sciences,Department of Molecular Genetics
[2] Human Cancer Genetics Program,Department of Molecular Virology Immunology and Medical Genetics
[3] Comprehensive Cancer Center,Department of Veterinary Biosciences
[4] ,undefined
[5] College of Medicine,undefined
[6] College of Veterinary Medicine,undefined
[7] and,undefined
[8] Center for Biostatistics,undefined
[9] The Ohio State University,undefined
[10] Columbus,undefined
[11] Ohio 43210,undefined
[12] USA ,undefined
[13] Present address: Department of Cell Biology and Molecular Medicine and University Hospital Cancer Center,undefined
[14] UMDNJ-New Jersey Medical School,undefined
[15] Newark,undefined
[16] New Jersey 07103,undefined
[17] USA.,undefined
来源
Nature | 2008年 / 454卷
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摘要
The E2F family is a family of proteins, some of which act as transcription activators and others as repressors. Here Shih-Yin Tsai et al. tested why there is such genetic complexity by inactivating the entire subset of activators singly or in combination in mice. They show that E2f3a is sufficient to support mouse embryonic and postnatal development. However, expression of E2f3b or E2f1 from the E2f3a locus suppressed all the postnatal phenotypes associated with the inactivation of E2f3a. They conclude there is functional redundancy among activators and that the requirement for E2f3a during postnatal development is dictated by its regulatory sequences, not by its protein function. These findings provide a molecular basis for the observed specificity among E2F activators during development.
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页码:1137 / 1141
页数:4
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