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Pleiotropic effects of HTLV type 1 Tax protein on cellular metabolism: mitotic checkpoint abrogation and NF-kappaB activation.

作者信息

Iha H, Kasai T, Kibler K V, Iwanaga Y, Tsurugi K, Jeang K T

机构信息

Laboratory of Molecular Microbiology, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.

出版信息

AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1633-8. doi: 10.1089/08892220050193074.

DOI:10.1089/08892220050193074
PMID:11080803
Abstract

Tax protein expressed by human T cell leukemia virus type 1 (HTLV-1) is a strong trans-activator of its own LTR promoter; it also affects the function of multiple cellular genes involved in cell cycle control and transcription. One way in which Tax exerts its pleiotropic effects is through protein-protein interaction with cellular cofactors. By using yeast two-hybrid technology, we have isolated several cellular proteins that bind to Tax. Two of these are MAD1, a mitotic checkpoint control protein, and TXBP151, a suppressor of tumor necrosis factor alpha-induced apoptosis. Here we discuss findings describing the role of MAD1 in exit of cells from mitosis and TXBP151 in NF-kappaB activation.

摘要

相似文献

1
Pleiotropic effects of HTLV type 1 Tax protein on cellular metabolism: mitotic checkpoint abrogation and NF-kappaB activation.
AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1633-8. doi: 10.1089/08892220050193074.
2
Coiled-coil motif as a structural basis for the interaction of HTLV type 1 Tax with cellular cofactors.
AIDS Res Hum Retroviruses. 2000 Nov 1;16(16):1689-94. doi: 10.1089/08892220050193155.
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Human T cell leukemia virus type 1 oncoprotein Tax targets the human mitotic checkpoint protein MAD1.人类1型T细胞白血病病毒癌蛋白Tax靶向人类有丝分裂检查点蛋白MAD1。
Cell. 1998 Apr 3;93(1):81-91. doi: 10.1016/s0092-8674(00)81148-4.
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HTLV-1 tax activation of the GM-CSF and G-CSF promoters requires the interaction of NF-kB with other transcription factor families.人嗜T淋巴细胞病毒1型(HTLV-1)的tax蛋白激活粒细胞-巨噬细胞集落刺激因子(GM-CSF)和粒细胞集落刺激因子(G-CSF)启动子需要核因子-κB(NF-κB)与其他转录因子家族相互作用。
Oncogene. 1993 Dec;8(12):3189-97.
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Overproduction of NFKB2 (lyt-10) and c-Rel: a mechanism for HTLV-I Tax-mediated trans-activation via the NF-kappa B signalling pathway.NFKB2(lyt-10)和c-Rel的过度产生:一种人嗜T淋巴细胞病毒I型Tax蛋白通过核因子κB信号通路介导反式激活的机制。
Oncogene. 1994 Mar;9(3):841-52.
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Human T-cell leukemia virus type I tax activates transcription of the human monocyte chemoattractant protein-1 gene through two nuclear factor-kappaB sites.人类I型T细胞白血病病毒的Tax蛋白通过两个核因子κB位点激活人单核细胞趋化蛋白-1基因的转录。
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Tax protein of HTLV-1 destabilizes the complexes of NF-kappa B and I kappa B-alpha and induces nuclear translocation of NF-kappa B for transcriptional activation.人类嗜T淋巴细胞病毒1型(HTLV-1)的Tax蛋白会使核因子κB(NF-κB)与κB抑制蛋白α(IκB-α)的复合物不稳定,并诱导NF-κB发生核转位以进行转录激活。
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Human T-cell leukemia virus type-I oncoprotein Tax inhibits Fas-mediated apoptosis by inducing cellular FLIP through activation of NF-kappaB.人类I型T细胞白血病病毒癌蛋白Tax通过激活核因子κB诱导细胞FLIP,从而抑制Fas介导的细胞凋亡。
Genes Cells. 2006 Feb;11(2):177-91. doi: 10.1111/j.1365-2443.2006.00927.x.

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