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人类嗜T细胞白血病Ⅰ型病毒(HTLV-I)是成人T细胞白血病(ATL)的致病因子,其编码的TAX蛋白的反式激活在白血病形成中有重要作用。NF-κB是细胞活化和产生细胞因子的重要转录调控因子。正常情况下,NF-κB因子与抑制性蛋白IKB结合,形成复合物存在于胞质中。TAX蛋白可与IKB激酶γ(IKKγ)直接结合,而后启动TAX对IKKα和IKKβ的结合,并使之发生磷酸化。后者使IKB蛋白降解,NF-κB获得释放,从胞质中转位到校内,与相应靶基因上的NF-κB位点结合而被活化,产生一系列生物性反应和效合作用。NF-κB因子具有拮抗细胞凋亡的作用,但其机制还有待深入研究。
Human T cell leukemia type 1 virus (HTLV-I) is a causative agent of adult T-cell leukemia (ATL) and transactivation of its encoded TAX protein plays an important role in the development of leukemia. NF-κB is an important transcriptional regulator of cell activation and production of cytokines. Normally, NF-κB binds to the inhibitory protein IKB, forming a complex in the cytoplasm. TAX protein binds directly to IKB kinase γ (IKKγ), and then initiates phosphorylation of TAK to IKKα and IKKβ. The latter degrades IKB protein, releases NF-κB, translocates from the cytoplasm to the inside of the cell, and binds to the NF-κB site on the corresponding target gene to be activated, resulting in a series of biological reactions and synergistic effects. NF-κB has the effect of antagonizing apoptosis, but its mechanism needs further study.