MALIGNANT TRANSFORMATION BY G-PROTEIN-COUPLED HORMONE RECEPTORS

被引：24

作者：

SHARIF, M

SASAKAWA, N

HANLEY, MR

机构：

[1] School of Medicine, Department of Biological Chemistry, University of California at Davis, Davis

来源：

MOLECULAR AND CELLULAR ENDOCRINOLOGY | 1994年 / 100卷 / 1-2期

关键词：

MALIGNANT TRANSFORMATION; HORMONE RECEPTOR; G PROTEIN;

D O I：

10.1016/0303-7207(94)90289-5

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

[No abstract available]

引用

页码：115 / 119

页数：5

共 42 条

[21]

KJELSBERG MA, 1992, J BIOL CHEM, V267, P1430

[22]

LAMORTE VJ, 1993, J BIOL CHEM, V268, P19411

[23] 2 MAJOR SIGNAL PATHWAYS LINKED [J].

MARX, J .

SCIENCE, 1993, 262 (5136) :988-&

[24] CDNA CLONING OF BOVINE SUBSTANCE-K RECEPTOR THROUGH OOCYTE EXPRESSION SYSTEM [J].

MASU, Y ;

NAKAYAMA, K ;

TAMAKI, H ;

HARADA, Y ;

KUNO, M ;

NAKANISHI, S .

NATURE, 1987, 329 (6142) :836-838

[25] SIGNAL TRANSDUCTION - HOW RECEPTORS TURN RAS ON [J].

MCCORMICK, F .

NATURE, 1993, 363 (6424) :15-16

[26]

MCDONNELL DP, 1993, BIO-TECHNOL, V11, P1256

[27] POINT MUTATION IN FGF RECEPTOR ELIMINATES PHOSPHATIDYLINOSITOL HYDROLYSIS WITHOUT AFFECTING MITOGENESIS [J].

MOHAMMADI, M ;

DIONNE, CA ;

LI, W ;

LI, N ;

SPIVAK, T ;

HONEGGER, AM ;

JAYE, M ;

SCHLESSINGER, J .

NATURE, 1992, 358 (6388) :681-684

[28] SOMATIC MUTATIONS IN THE THYROTROPIN RECEPTOR GENE CAUSE HYPERFUNCTIONING THYROID ADENOMAS [J].

PARMA, J ;

DUPREZ, L ;

VANSANDE, J ;

COCHAUX, P ;

GERVY, C ;

MOCKEL, J ;

DUMONT, J ;

VASSART, G .

NATURE, 1993, 365 (6447) :649-651

[29] POINT MUTATION OF AN FGF RECEPTOR ABOLISHES PHOSPHATIDYLINOSITOL TURNOVER AND CA2+ FLUX BUT NOT MITOGENESIS [J].

PETERS, KG ;

MARIE, J ;

WILSON, E ;

IVES, HE ;

ESCOBEDO, J ;

DELROSARIO, M ;

MIRDA, D ;

WILLIAMS, LT .

NATURE, 1992, 358 (6388) :678-681

[30] CHANGES IN INOSITOL LIPIDS AND PHOSPHATES AFTER STIMULATION OF THE MAS-TRANSFECTED NG115-401L-C3 CELL-LINE BY MITOGENIC AND NON-MITOGENIC STIMULI [J].

POYNER, DR ;

HAWKINS, PT ;

BENTON, HP ;

HANLEY, MR .

BIOCHEMICAL JOURNAL, 1990, 271 (03) :605-611

← 1 2 3 4 5 →