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The effects of a novel IB kinase (IKK) inhibitor, 2-amino-6-[2-(cyclopropylmethoxy)-6-hydroxyphenyl]-4-piperidin-4-yl nicotinonitrile (ACHP), were examined on cell growth of these cell lines and fresh ATL leukemic cells.We found that ACHP could inhibit the phosphorylation of IB and p65, as well as NF-B DNA-binding, associated with downregulation of the NF-B target genes and induce cell growth arrest and apoptosis in these cells.Correspondence: Professor T Okamoto, Department of Molecular and Cellular Biology, Nagoya City University Graduate School of Medical Sciences, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi 467-8601, Japan.
When Tax-active and Tax-inactive cell lines were compared, ACHP could preferentially inhibit cell growth of Tax-active cells.
Moreover, ACHP exhibited strong apoptosis-inducing activity in fresh ATL cells.
Conventional chemotherapies appeared to be ineffective in prolonging the life of patients with ATL, mostly due to the frequent acquisition of drug resistance and adverse effects.
Although novel clinical trials using interferon and arsenic trioxide or zidovudine exhibited better therapeutic responses, their efficacies were limited and only small percentages of patients achieved long-lasting remission.
NF-B is constitutively activated in adult T-cell leukemia (ATL) and is considered responsible for cell growth and prevention of cell death.
In this study, we demonstrate that NF-B is constitutively activated in various HTLV-1-infected T-cell lines and ATL-derived cell lines irrespectively of Tax expression as evidenced by the phosphorylation of IB and p65 subunit of NF-B, activation of NF-B DNA binding, and upregulation of various target genes including bcl-x, bcl-2, XIAP, c-IAP1, survivin, cyclin D1, ICAM-1 and VCAM-1.