C-FOS MESSENGER-RNA LEVELS ARE REDUCED IN THE PRESENCE OF ANTIPAIN AND BOWMAN-BIRK INHIBITOR

被引:32
作者
CAGGANA, M [1 ]
KENNEDY, AR [1 ]
机构
[1] UNIV PENN,SCH MED,SCH MED,DEPT RADIAT ONCOL,PHILADELPHIA,PA 19104
关键词
D O I
10.1093/carcin/10.11.2145
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
引用
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页码:2145 / 2148
页数:4
相关论文
共 29 条
[1]  
BILLINGS PC, 1988, CANCER RES, V48, P1798
[2]   A SERINE PROTEASE ACTIVITY IN C3H-10T1/2 CELLS THAT IS INHIBITED BY ANTICARCINOGENIC PROTEASE INHIBITORS [J].
BILLINGS, PC ;
CAREW, JA ;
KELLERMCGANDY, CE ;
GOLDBERG, AL ;
KENNEDY, AR .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1987, 84 (14) :4801-4805
[3]   INHIBITION OF RADIATION-INDUCED TRANSFORMATION OF C3H-10T1/2 CELLS BY CARBOXYPEPTIDASE INHIBITOR-1 AND INHIBITOR-II FROM POTATOES [J].
BILLINGS, PC ;
MORROW, AR ;
RYAN, CA ;
KENNEDY, AR .
CARCINOGENESIS, 1989, 10 (04) :687-691
[4]   CELL-CYCLE PROGRESSION OF C3H 10T1/2 AND 3T3 CELLS IN THE ABSENCE OF AN INCREASE IN C-MYC RNA LEVELS [J].
CHANG, JD ;
KENNEDY, AR .
CARCINOGENESIS, 1988, 9 (01) :17-20
[5]   C-MYC EXPRESSION IS REDUCED IN ANTIPAIN-TREATED PROLIFERATING C3H 10T1/2 CELLS [J].
CHANG, JD ;
BILLINGS, PC ;
KENNEDY, AR .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1985, 133 (02) :830-835
[6]  
CHANG JD, 1989, IN PRESS MOL CARCINO
[7]   ISOLATION OF BIOLOGICALLY-ACTIVE RIBONUCLEIC-ACID FROM SOURCES ENRICHED IN RIBONUCLEASE [J].
CHIRGWIN, JM ;
PRZYBYLA, AE ;
MACDONALD, RJ ;
RUTTER, WJ .
BIOCHEMISTRY, 1979, 18 (24) :5294-5299
[8]   EXPRESSION OF THE C-FOS GENE AND OF AN FOS-RELATED GENE IS STIMULATED BY PLATELET-DERIVED GROWTH-FACTOR [J].
COCHRAN, BH ;
ZULLO, J ;
VERMA, IM ;
STILES, CD .
SCIENCE, 1984, 226 (4678) :1080-1082
[9]   MULTIPLE PROTEIN-BINDING SITES IN THE 5'-FLANKING REGION REGULATE C-FOS EXPRESSION [J].
GILMAN, MZ ;
WILSON, RN ;
WEINBERG, RA .
MOLECULAR AND CELLULAR BIOLOGY, 1986, 6 (12) :4305-4316
[10]   THE HUMAN INTERFERON-BETA GENE ENHANCER IS UNDER NEGATIVE CONTROL [J].
GOODBOURN, S ;
BURSTEIN, H ;
MANIATIS, T .
CELL, 1986, 45 (04) :601-610