Proteins and Id2 converge on p57(Kip2) to regulate cell cycle in neural cells
文献类型：期刊论文
| 作者 | Rothschild G1; Zhao XD1; Iavarone A[*]1,2,3; Lasorella A1,2,4 |
| 刊名 | MOLECULAR AND CELLULAR BIOLOGY
 |
| 出版日期 | 2006 |
| 卷号 | 26期号:11页码:4351-4361 |
| 通讯作者 | ai2102@columbia.edu |
| 英文摘要 | A precise balance between proliferation and differentiation must be maintained during neural development to obtain the correct proportion of differentiated cell types in the adult nervous system. The basic helix-loop-helix (hHLH) transcription factors known as E proteins and their natural inhibitors, the Id proteins, control the timing of differentiation and terminal exit from the cell cycle. Here we show that progression into S phase of human neuroblastoma cells is prevented by E proteins and promoted by W. Cyclin-dependent kinase inhibitors (CKI) have been identified as key effectors of cell cycle arrest in differentiating cells. However, p57(Kip2) is the only CKI that is absolutely required for normal development. Through the use of global gene expression analysis in neuroblastoma cells engineered to acutely express the E protein E47 and W, we find that p57(Kip2) is a target of E47. Consistent with the role of Id proteins, Id2 prevents activation of p57(Kip2) expression, and the retinoblastoma tumor suppressor protein, a known Id2 inhibitor, counters this activity. The strong E47-mediated inhibition of entry into S phase is entirely reversed in cells in which expression of p57(Kip2) is silenced by RNA interference. During brain development, expression of p57(Kip2) is opposite that of Id2. Our findings identify p57(Kip2) as a functionally relevant target recruited by bHLH transcription factors to induce cell cycle arrest in developing neuroblasts and suggest that deregulated expression of Id proteins may be an epigenetic mechanism to silence expression of this CKI in neural tumors. |
| 收录类别 | SCI |
| 资助信息 | This work was supported by grants from NIH-NCI to A.L. (R01- CA101644) and A.I. (R01-CA85628) and from the Charlotte Geyer Foundation (A.I.). G.R. was supported by a training grant from the NIH (Ruth L. Kirschstein NRSA). |
| 语种 | 英语 |
| 公开日期 | 2014-07-07 |
| 源URL | [http://159.226.149.42:8088/handle/152453/7939]  |
| 专题 | 昆明动物研究所_科研共享资源 |
| 作者单位 | 1.Institute for Cancer Genetics, College of Physicians and Surgeons of Columbia University, New York, New York 10032 2.Department of Pathology, College of Physicians and Surgeons of Columbia University, New York, New York 10032 3.Department of Neurology, College of Physicians and Surgeons of Columbia University, New York, New York 10032 4.Department of Pediatrics,College of Physicians and Surgeons of Columbia University, New York, New York 10032 |
| 推荐引用方式 GB/T 7714 | Rothschild G,Zhao XD,Iavarone A[*],et al. Proteins and Id2 converge on p57(Kip2) to regulate cell cycle in neural cells[J]. MOLECULAR AND CELLULAR BIOLOGY,2006,26(11):4351-4361. |
| APA | Rothschild G,Zhao XD,Iavarone A[*],&Lasorella A.(2006).Proteins and Id2 converge on p57(Kip2) to regulate cell cycle in neural cells.MOLECULAR AND CELLULAR BIOLOGY,26(11),4351-4361. |
| MLA | Rothschild G,et al."Proteins and Id2 converge on p57(Kip2) to regulate cell cycle in neural cells".MOLECULAR AND CELLULAR BIOLOGY 26.11(2006):4351-4361. |
入库方式： OAI收割
来源：昆明动物研究所
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