Identification of NF‐jun, a novel inducible transcription factor that regulates c‐jun gene transcription.

In this study we report the identification of a novel transcription factor, termed Nuclear Factor‐jun (NF‐jun). This factor contributes to inducible transcription of the c‐jun gene in human myeloid leukemia cells. NF‐jun was, however, undetectable in nuclear proteins from human monocytes, granulocytes, resting T lymphocytes and lung fibroblasts. NF‐jun shares several features with the well characterized NF‐kappa B in that binding activity can be generated in cytosolic extracts by treatment with dissociating agents. In addition, binding of NF‐jun to its recognition site is enhanced by treatment of cells with 12‐O‐tetradecanoylphorbol‐13‐acetate, tumor necrosis factor alpha or the protein synthesis inhibitor cycloheximide (CHX). However, as revealed by competition assays and electrophoretic mobility shift assays, purified NF‐kappa B fails to bind to the c‐jun fragment which contains the NF‐jun site, and this fragment fails to compete with NF‐kappa B for binding. UV crosslinking showed that NF‐jun contains a 55 and a 125 kDa protein species. These findings demonstrate that the c‐jun gene can be regulated by a transcription factor distinct from AP‐1. Our findings also indicate that while NF‐jun has several features in common with the NF‐kappa B binding protein including its subcellular localization and its ability to translocate from the cytoplasm to the nucleus, this factor recognizes a unique DNA sequence. Moreover, the activity of this protein is differentially regulated in various cell types. NF‐jun might function as a signal transducing molecule in order to mediate rapid induction of the early response gene c‐jun in a cell type‐ and stimulus‐specific manner.