TRANSFORMING GROWTH-FACTOR-BETA EFFECTS ON EXPRESSION OF G(1) CYCLINS AND CYCLIN-DEPENDENT PROTEIN-KINASES

被引:290
作者
GENG, Y [1 ]
WEINBERG, RA [1 ]
机构
[1] MIT, DEPT BIOL, CAMBRIDGE, MA 02139 USA
关键词
CELL CYCLE PROGRESSION;
D O I
10.1073/pnas.90.21.10315
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Transforming growth factor beta1 (TGF-beta1) is a potent growth-inhibitory polypeptide. The mechanism of TGF-beta1 inhibition has been related to its ability to prevent the hyperphosphorylation of retinoblastoma protein (pRb). Several lines of evidence have suggested that cell cycle-regulated protein kinases are responsible for the hyperphosphorylation of pRb. We demonstrate here that TGF-beta1 has profound effects on the expression of genes encoding certain G1 cyclins and their associated kinases, which provides one explanation of TGF-beta1 effects on pRb hyperphosphorylation. These results also suggest that the growth-inhibitory effects of TGF-beta1 in many cells are attributable to its effects on the cell cycle apparatus involved in programming G1 transit.
引用
收藏
页码:10315 / 10319
页数:5
相关论文
共 35 条
[1]   NORMAL KERATINIZATION IN A SPONTANEOUSLY IMMORTALIZED ANEUPLOID HUMAN KERATINOCYTE CELL-LINE [J].
BOUKAMP, P ;
PETRUSSEVSKA, RT ;
BREITKREUTZ, D ;
HORNUNG, J ;
MARKHAM, A ;
FUSENIG, NE .
JOURNAL OF CELL BIOLOGY, 1988, 106 (03) :761-771
[2]   THE RETINOBLASTOMA PROTEIN IS PHOSPHORYLATED DURING SPECIFIC PHASES OF THE CELL-CYCLE [J].
BUCHKOVICH, K ;
DUFFY, LA ;
HARLOW, E .
CELL, 1989, 58 (06) :1097-1105
[3]   PHOSPHORYLATION OF THE RETINOBLASTOMA GENE-PRODUCT IS MODULATED DURING THE CELL-CYCLE AND CELLULAR-DIFFERENTIATION [J].
CHEN, PL ;
SCULLY, P ;
SHEW, JY ;
WANG, JYJ ;
LEE, WH .
CELL, 1989, 58 (06) :1193-1198
[4]   THE PRODUCT OF THE RETINOBLASTOMA SUSCEPTIBILITY GENE HAS PROPERTIES OF A CELL-CYCLE REGULATORY ELEMENT [J].
DECAPRIO, JA ;
LUDLOW, JW ;
LYNCH, D ;
FURUKAWA, Y ;
GRIFFIN, J ;
PIWNICAWORMS, H ;
HUANG, CM ;
LIVINGSTON, DM .
CELL, 1989, 58 (06) :1085-1095
[5]   CELL-CYCLE CONTROL IN EUKARYOTES - MOLECULAR MECHANISMS OF CDC2 ACTIVATION [J].
DRAETTA, G .
TRENDS IN BIOCHEMICAL SCIENCES, 1990, 15 (10) :378-383
[6]   ASSOCIATION OF HUMAN CYCLIN-E WITH A PERIODIC G(1)-S PHASE PROTEIN-KINASE [J].
DULIC, V ;
LEES, E ;
REED, SI .
SCIENCE, 1992, 257 (5078) :1958-1961
[7]  
FURUKAWA Y, 1992, J BIOL CHEM, V267, P17121
[8]   REGULATION OF RETINOBLASTOMA PROTEIN FUNCTIONS BY ECTOPIC EXPRESSION OF HUMAN CYCLINS [J].
HINDS, PW ;
MITTNACHT, S ;
DULIC, V ;
ARNOLD, A ;
REED, SI ;
WEINBERG, RA .
CELL, 1992, 70 (06) :993-1006
[9]   TRANSFORMING GROWTH FACTOR-BETA-1 INHIBITION OF P34CDC2 PHOSPHORYLATION AND HISTONE-H1 KINASE-ACTIVITY IS ASSOCIATED WITH G1/S-PHASE GROWTH ARREST [J].
HOWE, PH ;
DRAETTA, G ;
LEOF, EB .
MOLECULAR AND CELLULAR BIOLOGY, 1991, 11 (03) :1185-1194
[10]   CYCLINS AND CANCER [J].
HUNTER, T ;
PINES, J .
CELL, 1991, 66 (06) :1071-1074