Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1993 Dec;13(12):7429-38.
doi: 10.1128/mcb.13.12.7429-7438.1993.

Transformation by Fos proteins requires a C-terminal transactivation domain

R Wisdon  1 , I M Verma
Affiliations

Transformation by Fos proteins requires a C-terminal transactivation domain

R Wisdon et al. Mol Cell Biol. 1993 Dec.

Abstract

The Fos family of proteins now includes seven members: the retroviral proteins FBR-v-Fos and FBJ-v-Fos and the cellular proteins c-Fos, FosB, FosB2, Fra1, and Fra2. Four proteins (FBR-v-Fos, FBJ-v-Fos, c-Fos, and FosB) transform established rodent fibroblast cell lines, while three (FosB2, Fra1, and Fra2) do not. As all family members display sequence-specific DNA-binding activity as part of a heterodimeric complex with Jun proteins, other features must account for the differences in transforming potential. We demonstrate here that all transforming members have a C-terminal transactivation domain that is lacking in nontransforming members. The nontransforming proteins Fra1 and Fra2 can be converted to transforming proteins by fusion of a transactivation domain from either FosB or VP16. We also demonstrate that differences in the basic region-leucine zipper domain affecting either the affinity or sequence specificity of DNA binding are not determinants of the difference in transforming potential among members of the Fos family. The results further define the functional requirements for transformation by Fos proteins and suggest that the subunit composition of AP1 complexes is an important determinant of mitogenic signalling capability.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Eur J Biochem. 1980 Jun;107(2):303-14 - PubMed
    1. Cell. 1991 Feb 22;64(4):751-9 - PubMed
    1. Mol Cell Biol. 1982 Sep;2(9):1044-51 - PubMed
    1. Proc Natl Acad Sci U S A. 1984 Apr;81(7):1991-5 - PubMed
    1. Virology. 1984 May;135(1):229-43 - PubMed

Publication types

MeSH terms