INDUCTION OF APOPTOSIS BY THE C-MYC HELIX-LOOP HELIX/LEUCINE ZIPPER DOMAIN IN MOUSE 3T3-L1 FIBROBLASTS

被引：15

作者：

KOHLHUBER, F

HERMEKING, H

GRAESSMANN, A

EICK, D

机构：

[1] GSF MUNICH, FORSCHUNGSZENTRUM UMWELT & GESUNDHEIT, INST KLIN MOLEK BIOL & TUMORGENET, D-81377 MUNICH, GERMANY

[2] IMPERIAL CANC RES FUND, LONDON WC2A 3PX, ENGLAND

[3] FREE UNIV BERLIN, INST MOLEK BIOL & BIOCHEM, D-14195 BERLIN, GERMANY

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 1995年 / 270卷 / 48期

关键词：

D O I：

10.1074/jbc.270.48.28797

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The cellular proto-oncogene c-myc is involved in cell proliferation and transformation but is also implicated in the induction of programmed cell death (apoptosis). The c-Myc protein is a transcriptional activator with a carboxyl-terminal basic region/helix-loop-helix (HLH)/leucine zipper (LZ) domain. It forms heterodimers with the HLH/LZ protein Max and transactivates gene expression after binding DNA E-box elements. We have studied the phenotype of dominant negative mutants of c-Myc and Max in microinjection experiments. Max mutants with a deleted or mutated basic region inhibited DNA synthesis in serum stimulated 3T3-L1 mouse fibroblasts. In contrast, mutants of c-Myc expressing only the basic reson/HLH/LZ or HLH/LZ domains rapidly induced apoptosis at low and high serum levels. Co expression of the HLH/LZ domains of c-Myc and Max failed to do so. We suggest that the c-Myc HLH/LZ domain induces apoptosis by specific interaction with cellular factors different to Max.

引用

页码：28797 / 28805

页数：9

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