Molecular cloning of a cyclin-like protein associated with cyclin-dependent kinase 3 (cdk 3) in vivo

被引:33
作者
Matsuoka, M
Matsuura, Y
Semba, K
Nishimoto, I
机构
[1] Keio Univ, Sch Med, Dept Pharmacol, Shinjuku Ku, Tokyo 1608582, Japan
[2] Natl Inst Hlth, Lab Hepatatis Viruses 2, Shinjuku Ku, Tokyo 1628640, Japan
[3] Univ Tokyo, Inst Med Sci, Dept Cellular & Mol Biol, Minato Ku, Tokyo 1088639, Japan
关键词
D O I
10.1006/bbrc.2000.2965
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
cdk3 has been considered to be rate-limiting for cell cycle progression of mammalian cells while its precise function remains to be elucidated. To assess cdk3 function, a cDNA coding for a cyclin-like protein (designated as ik3-1 from an interactor-1 with cdk3) was isolated with the yeast two-hybrid system using a cyclin-dependent kinase 3 (cdk3) cDNA as bait. p70(ik3-1) (a 70-kDa protein designated as p70(ik3-1)) seems to belong to the cyclin family as its C-terminal domain composed of 124 amino acids resembles the highly conserved cyclin box. Coimmunoprecipitation indicated that p70(ik3-1) binds to p35(cdk3) in vivo. The ik3-1 gene may belong to a multigene family and is highly conserved during evolution. mRNA expression of ik3-1 was low in the early G1 phase, upregulated during G1 progression, maximal at a mid-late G1 point, and declined gradually thereafter, suggesting that it may work mainly in G1 phase. (C) 2000 Academic Press.
引用
收藏
页码:442 / 447
页数:6
相关论文
共 25 条
[1]
Human cyclin K, a novel RNA polymerase II-associated cyclin possessing both carboxy-terminal domain kinase and Cdk-activating kinase activity [J].
Edwards, MC ;
Wong, C ;
Elledge, SJ .
MOLECULAR AND CELLULAR BIOLOGY, 1998, 18 (07) :4291-4300
[2]
INHIBITION OF CYCLIN-DEPENDENT KINASES BY P21 [J].
HARPER, JW ;
ELLEDGE, SJ ;
KEYOMARSI, K ;
DYNLACHT, B ;
TSAI, LH ;
ZHANG, PM ;
DOBROWOLSKI, S ;
BAI, C ;
CONNELLCROWLEY, L ;
SWINDELL, E ;
FOX, MP ;
WEI, N .
MOLECULAR BIOLOGY OF THE CELL, 1995, 6 (04) :387-400
[3]
COLLABORATION OF G(1) CYCLINS IN THE FUNCTIONAL INACTIVATION OF THE RETINOBLASTOMA PROTEIN [J].
HATAKEYAMA, M ;
BRILL, JA ;
FINK, GR ;
WEINBERG, RA .
GENES & DEVELOPMENT, 1994, 8 (15) :1759-1771
[4]
Differential effects of cdk2 and cdk3 on the control of pRb and E2F function during G(1) exit [J].
Hofmann, F ;
Livingston, DM .
GENES & DEVELOPMENT, 1996, 10 (07) :851-861
[5]
TRAF5, a novel tumor necrosis factor receptor-associated factor family protein, mediates CD40 signaling [J].
Ishida, T ;
Tojo, T ;
Aoki, T ;
Kobayashi, N ;
Ohishi, T ;
Watanabe, T ;
Yamamoto, T ;
Inoue, J .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (18) :9437-9442
[6]
MECHANISM OF CDK ACTIVATION REVEALED BY THE STRUCTURE OF A CYCLINA-CDK2 COMPLEX [J].
JEFFREY, PD ;
RUSO, AA ;
POLYAK, K ;
GIBBS, E ;
HURWITZ, J ;
MASSAGUE, J ;
PAVLETICH, NP .
NATURE, 1995, 376 (6538) :313-320
[7]
CYCLIC-AMP-INDUCED G1 PHASE ARREST MEDIATED BY AN INHIBITOR (P27(KIP1)) OF CYCLIN-DEPENDENT KINASE-4 ACTIVATION [J].
KATO, JY ;
MATSUOKA, M ;
POLYAK, K ;
MASSAGUE, J ;
SHERR, CJ .
CELL, 1994, 79 (03) :487-496
[8]
IMPROVEMENTS IN PROTEIN SECONDARY STRUCTURE PREDICTION BY AN ENHANCED NEURAL NETWORK [J].
KNELLER, DG ;
COHEN, FE ;
LANGRIDGE, R .
JOURNAL OF MOLECULAR BIOLOGY, 1990, 214 (01) :171-182
[9]
Interferon-α-induced G1 phase arrest through up-regulated expression of CDK inhibitors, p19Ink4D and p21Cip1 in mouse macrophages [J].
Matsuoka, M ;
Tani, K ;
Asano, S .
ONCOGENE, 1998, 16 (16) :2075-2086
[10]
ACTIVATION OF CYCLIN-DEPENDENT KINASE-4 (CDK4) BY MOUSE MO15-ASSOCIATED KINASE [J].
MATSUOKA, M ;
KATO, JY ;
FISHER, RP ;
MORGAN, DO ;
SHERR, CJ .
MOLECULAR AND CELLULAR BIOLOGY, 1994, 14 (11) :7265-7275