IDENTIFICATION AND PROPERTIES OF AN ATYPICAL CATALYTIC SUBUNIT (P34(PSK-J3)/CDK4) FOR MAMMALIAN-D TYPE-G1 CYCLINS

被引：926
作者：
MATSUSHIME, H
EWEN, ME
STROM, DK
KATO, JY
HANKS, SK
ROUSSEL, MF
SHERR, CJ
机构：
[1] ST JUDE CHILDRENS RES HOSP, DEPT TUMOR CELL BIOL, MEMPHIS, TN 38105 USA
[2] UNIV TENNESSEE, CTR HLTH SCI, COLL MED, DEPT BIOCHEM, MEMPHIS, TN 38163 USA
[3] HARVARD UNIV, SCH MED, DANA FARBER CANC INST, BOSTON, MA 02115 USA
[4] VANDERBILT UNIV, MED CTR, SCH MED, NASHVILLE, TN 37232 USA
来源：
CELL | 1992年 / 71卷 / 02期
关键词：
D O I：
10.1016/0092-8674(92)90360-O
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：
Murine D type cyclins associate with a catalytic subunit (p34PSK-J3 with properties distinct from known cyclin-dependent kinases (cdks). Mouse p34PSK-J3 shows less than 50% amino acid identity to p34cdc2, p33cdk2, and p36cdk3, lacks a PSTAIRE motif, and does not bind to p13suc1. Cyclin D1-p34PSK-J3 complexes accumulate in macrophages during G1 and decline in S phase, whereas complexes involving cyclins D2 and D3 form in proliferating T cells. Although histone H1 kinase activity is not detected in cyclin D or PSK-J3 immunoprecipitates, cyclin D-p34PSK-J3 complexes assembled in vitro stably bind and phosphorylate the retinoblastoma gene product (pRb) and an Rb-like protein (p107) but do not interact with pRb mutants that are functionally inactive. Thus, p34PSK-J3 is a cyclin D-regulated catalytic subunit that acts as an Rb (but not H1) kinase.
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页码：323 / 334
页数：12
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