共 12 条
Master or slave: The complex relationship of RBP2 and pRb
被引:10
作者:

Gutierrez, GM
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机构: Tufts Univ, New England Med Ctr, Mol Oncol res Inst, Dept Radiat Oncol, Medford, MA 02155 USA

Kong, E
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机构: Tufts Univ, New England Med Ctr, Mol Oncol res Inst, Dept Radiat Oncol, Medford, MA 02155 USA

Hinds, PW
论文数: 0 引用数: 0
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机构:
Tufts Univ, New England Med Ctr, Mol Oncol res Inst, Dept Radiat Oncol, Medford, MA 02155 USA Tufts Univ, New England Med Ctr, Mol Oncol res Inst, Dept Radiat Oncol, Medford, MA 02155 USA
机构:
[1] Tufts Univ, New England Med Ctr, Mol Oncol res Inst, Dept Radiat Oncol, Medford, MA 02155 USA
[2] Tufts Univ, Sch Med, Grad Program Genet, Boston, MA 02154 USA
来源:
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D O I:
10.1016/j.ccr.2005.05.021
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
The retinoblastoma protein or its regulators are altered in most human cancers. Although commonly thought of as solely a repressor of E2F-dependent transcription and cell cycle progression, pRb has gained notoriety in recent years as a key actor in cellular differentiation programs. In the June issue of Molecular Cell, Benevolenskaya et al. report that a long-known but poorly understood pRb interactor, RBP2, acts as an inhibitor of differentiation contributing to pRb's role as a coordinator of differentiation and cell cycle exit. Loss of pRb may unleash RBP2, maintaining cells in a poorly differentiated progenitor state that is prerequisite to tumor formation.
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页码:501 / 502
页数:2
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