Rescue of cyclin D1 deficiency by knockin cyclin E

被引：281

作者：

Geng, Y

Whoriskey, W

Park, MY

Bronson, RT

Medema, RH

Li, TS

Weinberg, RA

Sicinski, P ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Dana Farber Canc Inst, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Dept Pathol, Boston, MA 02115 USA

[3] MIT, Whitehead Inst Biomed Res, Cambridge, MA 02142 USA

[4] MIT, Dept Biol, Cambridge, MA 02142 USA

[5] Tufts Univ, Sch Med & Vet Med, Boston, MA 02111 USA

[6] Univ Utrecht, Med Ctr, Jordan Lab, Dept Hematol, NL-3584 CX Utrecht, Netherlands

[7] Harvard Univ, Massachusetts Eye & Ear Infirm, Sch Med, Berman Gund Lab Study Retinal Degenerat, Boston, MA 02114 USA

来源：

CELL | 1999年 / 97卷 / 06期

关键词：

D O I：

10.1016/S0092-8674(00)80788-6

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

D-type cyclins and cyclin E represent two very distinct classes of mammalian G1 cyclins. We have generated a mouse strain in which the coding sequences of the cyclin D1 gene (Ccnd1) have been deleted and replaced by those of human cyclin E (CCNE). In the tissues and cells of these mice, the expression pattern of human cyclin E faithfully reproduces that normally associated with mouse cyclin D1. The replacement of cyclin D1 with cyclin E rescues all phenotypic manifestations of cyclin D1 deficiency and restores normal development in cyclin D1-dependent tissues. Thus, cyclin E can functionally replace cyclin D1. Our analyses suggest that cyclin E is the major downstream target of cyclin D1.

引用

页码：767 / 777

页数：11

共 25 条

[1] Cyclin E and c-Myc promote cell proliferation in the presence of p16(INK4a) and of hypophosphorylated retinoblastoma family proteins [J].