RNA polymerase III repression by the retinoblastoma tumor suppressor protein.
RNA polymerase III repression by the retinoblastoma tumor suppressor protein.
复制标题
RNA 聚合酶 III 受到视网膜母细胞瘤肿瘤抑制蛋白的抑制。
DOI：
10.1016/j.bbagrm.2012.09.011
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发表时间：
2013-03
影响因子：
4.7
通讯作者：
Henry, R. William
中科院分区：
文献类型：
--
作者：
Gjidoda, Alison;Henry, R. William
视网膜母细胞瘤（RB）肿瘤抑制蛋白调节影响细胞生长的多个途径，并且作为关键调节节点，其功能在大多数癌细胞中失活。除了其在细胞周期控制中的典型作用外，RB还作为RNA聚合酶（Pol）III转录的全局阻遏物发挥作用。事实上，Pol III转录物在癌细胞中积累，并且其升高的水平与RB功能障碍相关的加速生长有关。在这里，我们审查RB的阻遏不同类型的Pol III基因的机制。对于1型和2型基因，RB通过与核心转录机制（特别是Brf 1-TFIIIB）直接接触抑制转录，并抑制前起始复合物形成和Pol III募集。3型基因抑制的对比模型表明，RB调控涉及RB，一般的转录机制，包括SNAPc，和Pol III的稳定和同时启动子关联，这表明RB可能会阻碍Pol III启动子逃逸或延长。有趣的是，对RB和Pol III的已发表基因组关联数据的分析揭示了Pol III基因在活跃生长期间和与静止和衰老相关的停滞生长期间的调节复杂性。
The Retinoblastoma (RB) tumor suppressor protein regulates multiple pathways that influence cell growth, and as a key regulatory node, its function is inactivated in most cancer cells. In addition to its canonical roles in cell cycle control, RB functions as a global repressor of RNA polymerase (Pol) III transcription. Indeed, Pol III transcripts accumulate in cancer cells and their heightened levels are implicated in accelerated growth associated with RB dysfunction. Herein we review the mechanisms of RB repression for the different types of Pol III genes. For type 1 and type 2 genes, RB represses transcription through direct contacts with the core transcription machinery, notably Brf1-TFIIIB, and inhibits preinitiation complex formation and Pol III recruitment. A contrasting model for type 3 gene repression indicates that RB regulation involves stable and simultaneous promoter association by RB, the general transcription machinery including SNAPc, and Pol III, suggesting that RB may impede Pol III promoter escape or elongation. Interestingly, analysis of published genomic association data for RB and Pol III revealed added regulatory complexity for Pol III genes both during active growth and during arrested growth associated with quiescence and senescence.
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影响因子：
10.5
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Ford, E;Strubin, M;Hernandez, N
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Hernandez, N
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Henry, R. William
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