Date of Award

Spring 1994

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Department

Biological Sciences

Program/Concentration

Biomedical Sciences

Committee Director

Timothy J. Bos

Committee Member

Richard Stenberg

Committee Member

William Wasilenko

Committee Member

Frank Castora

Committee Member

Mark S. Elliot

Abstract

The v-jun oncogene was originally isolated from the ASV17 virus in 1987. Ever since its isolation, extensive work has been done to understand the role of the v-jun oncogene in cell transformation. The c-Jun protein is a transcription factor which binds to the DNA target TGACTCA. The c-Jun protein binds to DNA in the form of dimers. It can form homodimers with itself and heterodimers with Jun family (JunB and JunD), Fos family (FosB, Fra1 and Fra2), or with CREB family members through the leucine zipper motif. Because the c-jun proto-oncogene plays an important role in cell transformation, extensive work has been done to understand how it is regulated. Previously, it has been shown that c-jun transcription can be activated by growth factors, tumor promoters and other oncogenes such as ras and src. Regulation of c-jun activity has been studied at the level of transcription, dimerization, DNA binding and post-translational modification. I report here that the c-jun proto-oncogene can also be regulated at the translational level.

Comments

Dissertation submitted to the Faculty of Eastern Virginia Medical School and Old Dominion University in Partial Fulfillment of the Requirement for the Degree of Doctor of Philosophy in Biomedical Sciences.

DOI

10.25777/nx9c-mr35

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