共查询到20条相似文献,搜索用时 15 毫秒
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Klampfer L Huang J Swaby LA Augenlicht L 《The Journal of biological chemistry》2004,279(29):30358-30368
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TANK‐binding kinase 1 and Janus kinase 2 play important roles in the regulation of mitogen‐activated protein kinase phosphatase‐1 expression after toll‐like receptor 4 activation
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Eunji Kim Ju Y. Yoon Jongsung Lee Deok Jeong Jae G. Park Yo H. Hong Ji H. Kim Adithan Aravinthan Jong‐Hoon Kim Jae Y. Cho 《Journal of cellular physiology》2018,233(11):8790-8801
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Cytokine receptor common beta subunit-mediated STAT5 activation confers NF-kappa B activation in murine proB cell line Ba/F3 cells. 总被引:4,自引:0,他引:4
Tetsuya Nakamura Rika Ouchida Tsunenori Kodama Toshiyuki Kawashima Yuichi Makino Noritada Yoshikawa Sumiko Watanabe Chikao Morimoto Toshio Kitamura Hirotoshi Tanaka 《The Journal of biological chemistry》2002,277(8):6254-6265
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Suk K Chang I Kim YH Kim S Kim JY Kim H Lee MS 《The Journal of biological chemistry》2001,276(16):13153-13159
We investigated the molecular mechanism of the synergism between interferon gamma (IFNgamma) and tumor necrosis factor alpha (TNFalpha) documented in a variety of biological occasions such as tumor cell death and inflammatory responses. IFNgamma/TNFalpha synergistically induced apoptosis of ME-180 cervical cancer cells. IFNgamma induced STAT1 phosphorylation and interferon regulatory factor 1 (IRF-1) expression. Transfection of phosphorylation-defective STAT1 inhibited IFNgamma/TNFalpha-induced apoptosis, whereas IRF-1 transfection induced susceptibility to TNFalpha. Dominant-negative IkappaBalpha transfection sensitized ME-180 cells to TNFalpha. IFNgamma pretreatment attenuated TNFalpha- or p65-induced NF-kappaB reporter activity, whereas it did not inhibit p65 translocation or DNA binding of NF-kappaB. IRF-1 transfection alone inhibited TNFalpha-induced NF-kappaB activity, which was reversed by coactivator p300 overexpression. Caspases were activated by IFNgamma/TNFalpha combination; however, caspase inhibition did not abrogate IFNgamma/TNFalpha-induced cell death. Instead, caspase inhibitors directed IFNgamma/TNFalpha-treated ME-180 cells to undergo necrosis, as demonstrated by Hoechst 33258/propidium iodide staining and electron microscopy. Taken together, our results indicate that IFNgamma and TNFalpha synergistically act to destroy ME-180 tumor cells by either apoptosis or necrosis, depending on caspase activation, and STAT1/IRF-1 pathways initiated by IFNgamma play a critical role in IFNgamma/TNFalpha synergism by inhibiting cytoprotective NF-kappaB. IFNgamma/TNFalpha synergism appears to activate cell death machinery independently of caspase activation, and caspase activation seems to merely determine the mode of cell death. 相似文献
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Albrecht U Yang X Asselta R Keitel V Tenchini ML Ludwig S Heinrich PC Häussinger D Schaper F Bode JG 《Cellular signalling》2007,19(9):1866-1878
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Watcharasit P Bijur GN Song L Zhu J Chen X Jope RS 《The Journal of biological chemistry》2003,278(49):48872-48879