Skp2 is required for survival of aberrantly proliferating Rb1-deficient cells and for tumorigenesis in Rb1+/− mice

被引：0

作者：

Hongbo Wang

Frederick Bauzon

Peng Ji

Xiaoliang Xu

Daqian Sun

Joseph Locker

Rani S Sellers

Keiko Nakayama

Keiich I Nakayama

David Cobrinik

Liang Zhu

机构：

[1] The Albert Einstein Comprehensive Cancer Center and Liver Research Center,Department of Developmental and Molecular Biology and Medicine

[2] Albert Einstein College of Medicine,Department of Pathology

[3] Dyson Vision Research Institute,Department of Functional Genomics, Division of Developmental Genetics

[4] Weill-Cornell Medical College,Department of Molecular and Cellular Biology

[5] The Albert Einstein Comprehensive Cancer Center and Liver Research Center,undefined

[6] Albert Einstein College of Medicine,undefined

[7] Tohoku University Graduate School of Medicine,undefined

[8] Medical Institute of Bioregulation,undefined

[9] Kyushu University,undefined

[10] Present addresses: Whitehead Institute for Biomedical Research,undefined

[11] Cambridge,undefined

[12] Massachusetts,undefined

[13] USA (P.J.); Peptide Binding Laboratory,undefined

[14] The Salk Institute,undefined

[15] La Jolla,undefined

[16] California,undefined

[17] USA (H.W.); Departments of Pathology (X.X.) and Pediatrics (D.C.),undefined

[18] Memorial Sloan-Kettering Cancer Center,undefined

[19] New York,undefined

[20] New York,undefined

[21] USA.,undefined

来源：

Nature Genetics | 2010年 / 42卷

关键词：

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学科分类号：

摘要：

Liang Zhu and colleagues report that inactivation of Skp2, a target of the pRb tumor suppressor, completely prevented tumorigenesis in tumor-prone mice with loss of one Rb1 allele. This work nominates Skp2 as a drug target to combat Rb1-deficient tumors.

引用

页码：83 / 88

页数：5

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