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The zinc finger protein and transcriptional repressor Gfi1 as a regulator of the innate immune response

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机构: [1]Univ Klinikum Essen, Inst Zellbiol Tumorforsch, IFZ, D-45122 Essen, Germany [2]Inst Rech Clin Montreal, Montreal, PQ H2W 1R7, Canada [3]Univ Montreal, Dept Microbiol & Immunol, Dept Biochem, Montreal, PQ H2W 1R7, Canada [4]McGill Univ, Dept Biochem, Montreal, PQ H3A 2T5, Canada [5]McGill Univ, Div Expt Med, Montreal, PQ H3A 2T5, Canada [6]Beijing Ditan Hosp, Inst Infect Dis, Beijing 100011, Peoples R China [7]Capital Med Univ, Dept Resp Dis, Beijing Tongren Hosp, Beijing 100730, Peoples R China [8]Univ Klinikum Essen, Inst Pathol & Neuropathol, D-45122 Essen, Germany [9]Univ Klinikum Essen, Inst Mol Biol Tumorforsch, D-45122 Essen, Germany
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关键词: Gfi1 endotoxin apoptotsis Toll-like receptor inflammation innate immune response cytokines

摘要:
Gfi1 is a transcriptional repressor with a molecular weight between 47 and 55 kDa. The protein has six C-terminal C2H2-type zinc finger domains and a characteristic stretch of 20 amino acids, called the SNAG-domain, at its N-terminus. Expression of Gfi1 ranges from the hematopoietic and lymphoid system to sensory epithelia, lung and parts of the CNS. Gene knockout studies revealed that Gfi1 is essential for the development of granulocytes and plays a role in macrophage-dependent cytokine production, indicating that this protein shares the responsibility for different lines of defense against pathogens. Strikingly, Gfi1-deficient mice are highly sensitive to both endotoxin and bacterial infections and die rapidly after an experimental application of endotoxin or induction of infection with symptoms of septic shock. This sensitivity is mediated by an overproduction of tumor necrosis factor (TNF) and other inflammatory cytokines. The lung could be identified as the principal organ in which the accelerated inflammatory reactions take place in challenged Gfi1-deficient mice. Several lines of experimental evidence support a role of Gfi1 as a regulator of the Toll-like receptor (TLR) pathways, and, in general, as an essential modulator preventing an overshooting of the inflammatory response. (C) 2007 Elsevier GmbH. All rights reserved.

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出版当年[2007]版:
大类 | 3 区 医学
最新[2023]版:
大类 | 4 区 医学
小类 | 4 区 免疫学
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出版当年[2006]版:
Q3 IMMUNOLOGY
最新[2023]版:
Q3 IMMUNOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2006版] 出版当年五年平均 出版前一年[2005版] 出版后一年[2007版]

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第一作者机构: [1]Univ Klinikum Essen, Inst Zellbiol Tumorforsch, IFZ, D-45122 Essen, Germany [2]Inst Rech Clin Montreal, Montreal, PQ H2W 1R7, Canada [3]Univ Montreal, Dept Microbiol & Immunol, Dept Biochem, Montreal, PQ H2W 1R7, Canada [4]McGill Univ, Dept Biochem, Montreal, PQ H3A 2T5, Canada [5]McGill Univ, Div Expt Med, Montreal, PQ H3A 2T5, Canada [*1]Inst Rech Clin Montreal, 110 Ave Pins W Montreal, Montreal, PQ H2W 1R7, Canada
通讯作者:
通讯机构: [1]Univ Klinikum Essen, Inst Zellbiol Tumorforsch, IFZ, D-45122 Essen, Germany [2]Inst Rech Clin Montreal, Montreal, PQ H2W 1R7, Canada [3]Univ Montreal, Dept Microbiol & Immunol, Dept Biochem, Montreal, PQ H2W 1R7, Canada [4]McGill Univ, Dept Biochem, Montreal, PQ H3A 2T5, Canada [5]McGill Univ, Div Expt Med, Montreal, PQ H3A 2T5, Canada [*1]Inst Rech Clin Montreal, 110 Ave Pins W Montreal, Montreal, PQ H2W 1R7, Canada
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