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TGF-β1によるアポトーシス誘導におけるNF-κBとAP-1の役割：山村康子^1,2、Harvey F. Lodish¹(¹Whtite Head Institute、²東京医歯大・医院・感染分子制御)

Role of NF-κB and AP-1 in TGF-β1-induced apoptosis: Yasuko YAMAMURA^1,2 and Harvey F. LODISH¹ (¹Whitehead Institute, ²Dept. of Retroviral Regulation, Tokyo Medical and Dental Univ.)

Transforming growth factor-β1 (TGF-β1), a member of the TGF-β superfamily, regulates cell growth, differentiation, and apoptosis. Although Smad proteins are identified transducers of the TGF-β signaling for cell growth arrest and embryonal pattern formation, little is known about signaling for apoptosis. Recent reports show that activity of NF-κB and (or) AP-1 controls apoptosis induced by TNFα, growth factor-withdrawal, and DNA damage. To address the role of these transcription factors in TGF-β1-induced apoptosis, we examined their DNA binding activities by gelshift assays in M1 myeloid cells which undergo apoptosis following TGF-β1 treatment. A 48hr treatment of M1 cells with TGF-β1 resulted in a dramatic increase in AP-1 binding activity and apoptosis. Only minor alterations were observed in NF-κB binding activity. Results of supershift assays and overexpression experiments of NF-κB and AP-1 components will be discussed.