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Background: c-Jun is a major component of the heterodimeric transcription factor AP-1 and is essential for embryonic development (1). It mediates several cellular processes, including proliferation and survival, and is upregulated in many carcinomas (2). Transactivation of c-Jun is regulated by Jun-N-terminal Kinases (JNKs) through phosphorylation at Serine 63 and 73, as well as at threonine 91 and 93 (3). Evidence supports that phosphorylation in NH2-terminal residues of c-Jun stimulates the dephosphorylation of the COOH-terminal sites, and consequently increases the DNA-binding activity of the transcription factor (4). c-Jun N-terminal kinase (JNK) isoforms are required for the phosphorylation of Threonine 91 and 93 in response to anisomycin in macrophages and TNF-alpha or anisomycin in fibroblasts (5).