The retinoblastoma protein and the cell cycle.
The retinoblastoma protein and the cell cycle.
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DOI：
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发表时间：
1992-06
影响因子：
14.5
通讯作者：
M. Sopta;B. Gallie;Gill Rm;P. Hamel;M. Muncaster;E. Zacksenhaus;R. A. Phillips
中科院分区：
文献类型：
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作者：
M. Sopta;B. Gallie;Gill Rm;P. Hamel;M. Muncaster;E. Zacksenhaus;R. A. Phillips
虽然视网膜母细胞瘤基因(RB1)突变在许多类型的肿瘤中起到恶性进展的作用，但RB1突变在癌症发生中的作用仅限于罕见的胚胎肿瘤-视网膜母细胞瘤。然而，在许多组织中，RB1是表达的，其产物p110RB1通过细胞周期进行调节。P110RB1作为细胞周期基因转录调节器的新证据可能澄清了这一表面上的悖论。组织特异性效应可能由与p110RB1相互作用的细胞蛋白决定，或由p110RB1调控的靶基因的细胞类型特异性表达决定。
Although mutations of the retinoblastoma gene (RB1) contribute to malignant progression in many types of tumor, the role of RB1 mutation in cancer initiation is highly restricted to the rare embryonic tumor, retinoblastoma. However, RB1 is expressed and its product, p110RB1, is regulated through the cell cycle in many tissues. This apparent paradox may be clarified by the emerging evidence that p110RB1 functions as a regulator of transcription of cell cycle genes. Tissue specific effects may be determined by the cellular proteins that interact with p110RB1, or by cell type-specific expression of target genes regulated by p110RB1.