抄録
The cyclin-dependent kinase inhibitors (CKIs) p27 and p57 are structurally similar, and their biochemical and cellular functions have been thought to be equivalent. However, mice deficient in either p27 or p57 exhibit markedly different phenotypes, suggesting that the in vivo roles of these two proteins might differ. To address this apparent discrepancy, we have generated a knock-in mouse model in which the endogenous p57 gene is replaced by the p27 gene, with p27 thus being expressed instead of p57. This mouse model has provided evidence that p57 functions as a bona fide CKI in vivo and that most of its roles can be performed by p27. Our findings also highlight and provide insight into the question of what determines the distinct cellular responses to abnormal cell cycling induced by the loss of CKIs.
| 元の言語 | 英語 |
|---|---|
| ページ（範囲） | 2497-2501 |
| ページ数 | 5 |
| ジャーナル | Cell Cycle |
| 巻 | 8 |
| 発行部数 | 16 |
| DOI | |
| 出版物ステータス | 出版済み - 8 15 2009 |
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All Science Journal Classification (ASJC) codes
- Molecular Biology
- Developmental Biology
- Cell Biology
これを引用
Functional similarities and uniqueness of p27 and p57 : Insight from a knock-in mouse model. / Susaki, Etsuo; Nakayama, Keiichi.
：: Cell Cycle, 巻 8, 番号 16, 15.08.2009, p. 2497-2501.研究成果: ジャーナルへの寄稿 › 評論記事
}
TY - JOUR
T1 - Functional similarities and uniqueness of p27 and p57
T2 - Insight from a knock-in mouse model
AU - Susaki, Etsuo
AU - Nakayama, Keiichi
PY - 2009/8/15
Y1 - 2009/8/15
N2 - The cyclin-dependent kinase inhibitors (CKIs) p27 and p57 are structurally similar, and their biochemical and cellular functions have been thought to be equivalent. However, mice deficient in either p27 or p57 exhibit markedly different phenotypes, suggesting that the in vivo roles of these two proteins might differ. To address this apparent discrepancy, we have generated a knock-in mouse model in which the endogenous p57 gene is replaced by the p27 gene, with p27 thus being expressed instead of p57. This mouse model has provided evidence that p57 functions as a bona fide CKI in vivo and that most of its roles can be performed by p27. Our findings also highlight and provide insight into the question of what determines the distinct cellular responses to abnormal cell cycling induced by the loss of CKIs.
AB - The cyclin-dependent kinase inhibitors (CKIs) p27 and p57 are structurally similar, and their biochemical and cellular functions have been thought to be equivalent. However, mice deficient in either p27 or p57 exhibit markedly different phenotypes, suggesting that the in vivo roles of these two proteins might differ. To address this apparent discrepancy, we have generated a knock-in mouse model in which the endogenous p57 gene is replaced by the p27 gene, with p27 thus being expressed instead of p57. This mouse model has provided evidence that p57 functions as a bona fide CKI in vivo and that most of its roles can be performed by p27. Our findings also highlight and provide insight into the question of what determines the distinct cellular responses to abnormal cell cycling induced by the loss of CKIs.
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UR - http://www.scopus.com/inward/citedby.url?scp=69249232305&partnerID=8YFLogxK
U2 - 10.4161/cc.8.16.9330
DO - 10.4161/cc.8.16.9330
M3 - Review article
C2 - 19597343
AN - SCOPUS:69249232305
VL - 8
SP - 2497
EP - 2501
JO - Cell Cycle
JF - Cell Cycle
SN - 1538-4101
IS - 16
ER -