The regulation of cyclin D1 degradation: roles in cancer development and the potential for therapeutic invention.

The regulation of cyclin D1 degradation: roles in cancer development and the potential for therapeutic invention.
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细胞周期蛋白D1降解的调节:在癌症发展中的作用和治疗发明的可能性。

DOI:
10.1186/1476-4598-6-24
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发表时间:
2007-04-02
期刊:
影响因子:
37.3
通讯作者:
Alao, John P.
Alao, John P.
中科院分区:
医学1区
文献类型:
--
作者:
Alao, John P.

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细胞周期蛋白D1是细胞周期进程的重要调节因子,并可作为转录辅助调节因子发挥作用。细胞周期蛋白D1的过度表达与癌症的发生和发展有关。细胞周期蛋白D1降解失调似乎是导致几种癌症中细胞周期蛋白D1水平升高的原因。最近的研究结果已经确定了新的机制参与调节细胞周期蛋白D1的稳定性。许多治疗剂已显示诱导细胞周期蛋白D1降解。对细胞周期蛋白D1的治疗性消融可能有助于癌症的预防和治疗。在这篇综述中,目前的知识对细胞周期蛋白D1降解的调节进行了讨论。新的见解细胞周期蛋白D1降解的消融治疗的背景下也进行了讨论。一些悬而未决的问题,关于细胞周期蛋白D1水平的调节也得到了解决。
Cyclin D1 is an important regulator of cell cycle progression and can function as a transcriptionl co-regulator. The overexpression of cyclin D1 has been linked to the development and progression of cancer. Deregulated cyclin D1 degradation appears to be responsible for the increased levels of cyclin D1 in several cancers. Recent findings have identified novel mechanisms involved in the regulation of cyclin D1 stability. A number of therapeutic agents have been shown to induce cyclin D1 degradation. The therapeutic ablation of cyclin D1 may be useful for the prevention and treatment of cancer. In this review, current knowledge on the regulation of cyclin D1 degradation is discussed. Novel insights into cyclin D1 degradation are also discussed in the context of ablative therapy. A number of unresolved questions regarding the regulation of cellular cyclin D1 levels are also addressed.
DOI: 10.1158/1078-0432.ccr-04-1023
发表时间: 2004-12-01
影响因子: 11.5
作者:
Alao, JP;Lam, EWF;Vigushin, DM
通讯作者: Vigushin, DM
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期刊: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES
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DOI: 10.1002/ijc.20774
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组蛋白脱乙酰基酶抑制剂trichostatin A在MCF-7乳腺癌细胞中诱导泛素依赖性细胞周期蛋白D1降解。
DOI: 10.1186/1476-4598-5-8
发表时间: 2006-02-20
期刊: MOLECULAR CANCER
影响因子: 37.3
作者:
Alao, John P;Stavropoulou, Alexandra V;Lam, Eric W-F;Coombes, R Charles;Vigushin, David M
通讯作者: Vigushin, David M