GROWTH-INHIBITION BY TRANSFORMING GROWTH FACTOR-BETA(TGF-BETA) TYPE-I IS RESTORED IN TGF-BETA-RESISTANT HEPATOMA-CELLS AFTER EXPRESSION OF TGF-BETA RECEPTOR TYPE-II CDNA

被引：209
|
作者：
INAGAKI, M
MOUSTAKAS, A
LIN, HY
LODISH, HF
CARR, BI
机构：
[1] UNIV PITTSBURGH,PITTSBURGH TRANSPLANTAT INST,PITTSBURGH,PA 15260
[2] WHITEHEAD INST BIOMED RES,CAMBRIDGE,MA 02142
[3] MIT,DEPT BIOL,CAMBRIDGE,MA 02139
来源：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 1993年 / 90卷 / 11期
关键词：
HUMAN HEPATOMA; TRANSFECTION; POLYCLONAL ANTISERA;
D O I：
10.1073/pnas.90.11.5359
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：
The growth of human hepatoma Hep 3B cells is potently inhibited by TGF-beta1 (ID50 = 0.2 ng/ml, 8 pM). A mutant cell line was derived that was not inhibited in growth by TGF-beta1 at 5 ng/ml (200 pM) and that lacked TGF-beta receptor type II (TGF-betaRII) gene. Transfection of the cloned cDNA for human TGF-betaRII to this mutant cell line restored receptor expression as well as the inhibition in growth by TGF-beta1. In both wild-type and mutant cells stably transfected with TGF-betaRII cDNA, TGF-betaRII coimmunoprecipitated with TGF-beta receptor type I in the presence of ligand. These experiments provide direct evidence for the role of TGF-betaRII in the inhibitory effect of TGF-beta on growth and suggest that TGF-betaRII acts by means of a heteromeric surface complex with TGF-beta receptor type I.
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页码：5359 / 5363
页数：5
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