The c-Jun-Induced Transformation Process Involves Complex Regulation of Tenascin-C Expression†

Interleukin‐1β impairment of transforming growth factor β1 signaling by DOWN‐REGULATION of transforming growth factor β receptor type II and up‐regulation of Smad7 in human articular chondrocytes

“…Therefore, although putative sites for AP-1 have been described in the human TGF␤RII promoter (46), AP-1 proteins could act through other sites. For example, AP-1 protein has previously been shown to cooperate individually with RelA proteins at the NF-B site of the promoter of specific cellular genes (47,48). However, it is not clear whether p65 and AP-1 were recruited to the native TGF␤RII promoter.…”

Transcriptional Regulation of the Endogenous Danger Signal Tenascin-C: A Novel Autocrine Loop in Inflammation

“…The induction of tenascin-C in MDDCs is NF-kB dependent; this is the first transcription factor identified that is able to drive endogenous tenascin-C expression. Transfection of c-Jun into rat embryonic fibroblasts activated a construct comprising the 2220 to +79-bp fragment of the basal promoter, and this required synergistic binding of NFkB and c-Jun (47), supporting the importance of NF-kB in controlling tenascin-C transcription. We found 33 putative NF-kB binding sites in conserved noncoding sequences within the 59 region of the tenascin-C gene and in the first intron (known to be important for cell-specific induction of the gene); putative binding sites in other conserved noncoding sequences may also exist.…”

Functional cooperation between JunD and NF-κB in rat hepatocytes

“…Jun proteins therefore appear to participate to the formation of highly organized complexes of transcription factors thus providing a potent means of amplifying gene responses. Previous identi®cation of AP-1 proteins cooperating individually with Rel proteins on the NFkB site of the promoter of speci®c cellular genes, such as the tenascin gene, or the HIV-1 gene have been provided (Mettouchi et al, 1997;Yang et al, 1999). In HeLa cells and F9 embryonal carcinoma cells, cFos and c-Jun but not JunB or JunD were found to synergize for NF-kB cooperation (Stein et al, 1993).…”