A potential role for p15Ink4b and p57Kip2 in liver development

FEBS Letters

Sanders, Jennifer A¹  Gruppuso, Philip A¹  Awad, Michael M¹ 

[1] Department of Pediatrics, Rhode Island Hospital and Brown University School of Medicine, 593 Eddy Street, Providence, RI 02903, USA

关键词: Hepatocyte;    Fetal;    Cell cycle;    p15Ink4b;    p21Cip1;    p57Kip2;    CDK;    cyclin-dependent kinase;    CKI;    cyclin-dependent kinase inhibitor;    RT-PCR;    reverse transcriptase-polymerase chain reaction;    TGFβ;    transforming growth factor-β;   

DOI  :  10.1016/S0014-5793(00)02108-6

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Hepatocytes undergo marked changes in proliferation during normal liver development. In order to elucidate the mechanism for these changes, we examined the ontogeny of expression for the known cyclin-dependent kinase inhibitors (CKIs), p15^Ink4b, p16^Ink4a, p18^Ink4c, p19^Ink4d, p21^Cip1, p27^Kip1 and p57^Kip2. All except p16^Ink4a were expressed at some time between late gestation and adulthood. The mRNA and protein expression patterns for p15^Ink4b and p57^Kip2 were consistent with a role for these CKIs in the regulation of hepatocyte proliferation. Specifically, p57^Kip2 may contribute to hepatocyte growth arrest that occurs in term fetuses, while p15^Ink4b may contribute to the maintenance of adult hepatocytes in a quiescent state. These results assign a possible role to two CKIs not previously identified as involved in hepatocyte cell cycle control.

【 授权许可】

Unknown