FAILURE OF WILD-TYPE OR A MUTANT FORM OF PROTEIN KINASE-C-ALPHA TO TRANSFORM FIBROBLASTS

被引:81
作者
BORNER, C
FILIPUZZI, I
WEINSTEIN, IB
IMBER, R
机构
[1] COLUMBIA UNIV,CTR COMPREHENS CANC,NEW YORK,NY 10032
[2] COLUMBIA UNIV,INST CANC RES,NEW YORK,NY 10032
[3] UNIV BASEL CLIN,SCH MED,MOLEC TUMORBIOL LAB,CH-4031 BASEL,SWITZERLAND
关键词
D O I
10.1038/353078a0
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
A MUTANT form of the alpha-isoform of protein kinase C (PKC) was recently isolated from an ultraviolet radiation-induced murine fibrosarcoma cell line and reported to transform mouse BALB/c 3T3 fibroblasts on transfection 1. Four point mutations in the regulatory domain were assumed to be responsible for its oncogenicity and unusual preference for membrane localization. Here, we report that overexpression of the reported mutant PKC-alpha complementary DNA in three fibroblast cell lines, including BALB/c 3T3, does not enable these cells to grow in soft agar or nude mice. In addition, this mutant PKC-alpha form seems to be indistinguishable from the wild-type PKC-alpha with respect to its dependence on cofactors, phorbol ester binding, subcellular distribution and its effects on growth and morphology. These results fail to confirm the previous study 1 and indicate that overexpression of either the wild-type or the reported mutant form of PKC-alpha does not transform rodent fibroblasts.
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页码:78 / 80
页数:3
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