title: [Anti-AP-1 treatment].
abstract: This review emphasizes our first discovery on the contribution of over-activation of c-fos gene to the pathogenesis of rheumatoid joint destruction. In particular, c-Fos signalling was required for increased activity of synovial mesenchymal cells which finally leads to rheumatoid joint destruction and peri-articular osteoporosis. Over-activation of c-fos via Wee1 kinase is responsible for tumor-like synovial over-growth. Our team designed anti-c-Fos drugs that specifically inhibit action of c-Fos at the AP-1 consensus sequence by using a computer-assisted drug design, which was the front-runner work executed in Japan.
authors.affiliation: Department of Rheumatology, Kobe University Graduate School of Medicine Kobe University Hospital.
authors.forename: Shunichi
authors.initials: S
authors.lastname: Shiozawa
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Narita
authors.forename: Shuichi
authors.initials: S
authors.lastname: Hirono
mesh_terms: D001172:Arthritis, Rheumatoid / Q000188:drug therapy*; D017076:Computer-Aided Design; D015195:Drug Design; D016762:Genes, fos / Q000502:physiology; D006801:Humans; D018808:Transcription Factor AP-1 / Q000037:antagonists & inhibitors*
chemical_list: D018808:Transcription Factor AP-1