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本文引用的文献

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Pyrin inflammasome activation and RhoA signaling in the autoinflammatory diseases FMF and HIDS.自身炎症性疾病家族性地中海热(FMF)和高免疫球蛋白D综合征(HIDS)中的吡啉炎性小体激活和RhoA信号传导
Nat Immunol. 2016 Aug;17(8):914-21. doi: 10.1038/ni.3457. Epub 2016 Jun 6.
2
Control of the innate immune response by the mevalonate pathway.甲羟戊酸途径对先天性免疫反应的调控
Nat Immunol. 2016 Aug;17(8):922-9. doi: 10.1038/ni.3487. Epub 2016 Jun 6.
3
Familial autoinflammation with neutrophilic dermatosis reveals a regulatory mechanism of pyrin activation.家族性中性粒细胞皮肤病性自身炎症揭示了 pyrin 激活的调控机制。
Sci Transl Med. 2016 Mar 30;8(332):332ra45. doi: 10.1126/scitranslmed.aaf1471.
4
14-3-3 proteins in plant-pathogen interactions.植物-病原体相互作用中的14-3-3蛋白
Mol Plant Microbe Interact. 2015 May;28(5):511-8. doi: 10.1094/MPMI-10-14-0322-CR.
5
An updated view on the structure and function of PYRIN domains.关于吡啉结构域的结构与功能的最新观点。
Apoptosis. 2015 Feb;20(2):157-73. doi: 10.1007/s10495-014-1065-1.
6
Innate immune sensing of bacterial modifications of Rho GTPases by the Pyrin inflammasome.先天免疫感应 Pyrin 炎症小体对 Rho GTPases 的细菌修饰
Nature. 2014 Sep 11;513(7517):237-41. doi: 10.1038/nature13449. Epub 2014 Jun 11.
7
How complex are intracellular immune receptor signaling complexes?细胞内免疫受体信号复合物有多复杂?
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Horror autoinflammaticus: the molecular pathophysiology of autoinflammatory disease (*).自身炎症恐怖症:自身炎症性疾病的分子病理生理学(*)
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Interaction of pyrin with 14.3.3 in an isoform-specific and phosphorylation-dependent manner regulates its translocation to the nucleus.吡喃素与14-3-3以异构体特异性和磷酸化依赖性方式相互作用,调节其向细胞核的转位。
Arthritis Rheum. 2005 Jun;52(6):1848-57. doi: 10.1002/art.21050.

对吡喃素炎性小体激活的剧烈RHOA阻断

A dRAStic RHOAdblock of Pyrin inflammasome activation.

作者信息

Dorfleutner Andrea, Stehlik Christian

机构信息

Division of Rheumatology, Department of Medicine, Feinberg School of Medicine, Robert H. Lurie Comprehensive Cancer Center, Interdepartmental Immunobiology Center and Skin Disease Research Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.

出版信息

Nat Immunol. 2016 Jul 19;17(8):900-2. doi: 10.1038/ni.3511.

DOI:10.1038/ni.3511
PMID:27434003
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5110454/
Abstract

The Pyrin inflammasome guard is disabled if the activity of small cellular GTPase is compromised, in response to defects in the mevalonate pathway and directly by mutations in Pyrin, resulting in the IL-1β-driven autoinflammatory diseases MKD and FMF.

摘要

如果小细胞GTP酶的活性受到损害,响应甲羟戊酸途径缺陷并直接由 Pyrin 突变,Pyrin炎性小体保护机制就会失效,从而导致由白细胞介素-1β驱动的自身炎症性疾病MKD和FMF。