螺旋组装在死亡域（DD）超家族中。
Helical assembly in the death domain (DD) superfamily.
机构信息
Department of Biochemistry, Weill Cornell Medical College and Graduate School of Medical Sciences, New York, NY 10021, USA.
出版信息
Curr Opin Struct Biol. 2012 Apr;22(2):241-7. doi: 10.1016/j.sbi.2012.02.006. Epub 2012 Mar 17.
Abstract
Death domain (DD) superfamily members play a central role in apoptotic and inflammatory signaling through formation of oligomeric molecular scaffolds. These scaffolds promote the activation of proinflammatory and apoptotic initiator caspases, as well as Ser/Thr kinases. Interactions between DDs are facilitated by a conserved set of interaction surfaces, type I, type II, and type III. Recently structural information on a ternary complex containing the DDs of MyD88, IRAK4, and IRAK2 and a binary complex containing Fas and FADD DDs has become available. This review will focus on how the three DD interaction surfaces cooperate to facilitate the assembly of these oligomeric signaling complexes.
摘要
死亡结构域（DD）超家族成员通过形成寡聚分子支架，在凋亡和炎症信号中发挥核心作用。这些支架促进炎症和凋亡起始半胱氨酸蛋白酶的激活，以及 Ser/Thr 激酶的激活。DD 之间的相互作用是通过一组保守的相互作用表面，即 I 型、II 型和 III 型来促进的。最近，含有 MyD88、IRAK4 和 IRAK2 的 DD 的三元复合物以及含有 Fas 和 FADD DD 的二元复合物的结构信息已经可用。这篇综述将重点介绍这三个 DD 相互作用表面如何协同作用，促进这些寡聚信号复合物的组装。
相似文献
1
Helical assembly in the death domain (DD) superfamily.螺旋组装在死亡域（DD）超家族中。
Curr Opin Struct Biol. 2012 Apr;22(2):241-7. doi: 10.1016/j.sbi.2012.02.006. Epub 2012 Mar 17.
2
Helical assembly in the MyD88-IRAK4-IRAK2 complex in TLR/IL-1R signalling.TLR/IL-1R 信号转导中 MyD88-IRAK4-IRAK2 复合物的螺旋组装。
Nature. 2010 Jun 17;465(7300):885-90. doi: 10.1038/nature09121. Epub 2010 May 19.
3
Structural study of the RIPoptosome core reveals a helical assembly for kinase recruitment.RIPoptosome核心的结构研究揭示了一种用于激酶招募的螺旋组装结构。
Biochemistry. 2014 Aug 26;53(33):5424-31. doi: 10.1021/bi500585u. Epub 2014 Aug 13.
4
Death domain assembly mechanism revealed by crystal structure of the oligomeric PIDDosome core complex.寡聚PIDDosome核心复合物晶体结构揭示死亡结构域组装机制。
Cell. 2007 Feb 9;128(3):533-46. doi: 10.1016/j.cell.2007.01.019.
5
Formation of the death domain complex between FADD and RIP1 proteins in vitro.体外FADD与RIP1蛋白之间死亡结构域复合物的形成。
Biochim Biophys Acta. 2013 Jan;1834(1):292-300. doi: 10.1016/j.bbapap.2012.08.013. Epub 2012 Aug 19.
6
Two human MYD88 variants, S34Y and R98C, interfere with MyD88-IRAK4-myddosome assembly.两种人类 MYD88 变异体，S34Y 和 R98C，干扰 MYD88-IRAK4-衔接子复合物的组装。
J Biol Chem. 2011 Jan 14;286(2):1341-53. doi: 10.1074/jbc.M110.159996. Epub 2010 Oct 21.
7
Flexible stoichiometry and asymmetry of the PIDDosome core complex by heteronuclear NMR spectroscopy and mass spectrometry.通过异核核磁共振光谱法和质谱法研究PIDDosome核心复合物的灵活化学计量和不对称性。
J Mol Biol. 2015 Feb 27;427(4):737-752. doi: 10.1016/j.jmb.2014.11.021. Epub 2014 Dec 18.
8
Structural insight for the roles of fas death domain binding to FADD and oligomerization degree of the Fas-FADD complex in the death-inducing signaling complex formation: a computational study.结构洞察 Fas 死亡结构域与 FADD 的结合以及 Fas-FADD 复合物的寡聚化程度在死亡诱导信号复合物形成中的作用：一项计算研究。
Proteins. 2013 Mar;81(3):377-85. doi: 10.1002/prot.24193. Epub 2012 Nov 5.
9
Direct binding of Fas-associated death domain (FADD) to the tumor necrosis factor-related apoptosis-inducing ligand receptor DR5 is regulated by the death effector domain of FADD.Fas相关死亡结构域（FADD）与肿瘤坏死因子相关凋亡诱导配体受体DR5的直接结合受FADD死亡效应结构域的调控。
J Biol Chem. 2004 Jul 30;279(31):32780-5. doi: 10.1074/jbc.M401680200. Epub 2004 Jun 1.
10
Identification of an expanded binding surface on the FADD death domain responsible for interaction with CD95/Fas.鉴定FADD死亡结构域上负责与CD95/Fas相互作用的扩展结合表面。
J Biol Chem. 2004 Jan 9;279(2):1474-81. doi: 10.1074/jbc.M304996200. Epub 2003 Oct 22.
引用本文的文献
1
A histidine switch regulates pH-dependent filament formation by the caspase-9 CARD.一个组氨酸开关通过半胱天冬酶-9的CARD结构域调节pH依赖性的丝状结构形成。
bioRxiv. 2025 Jun 3:2025.06.02.657148. doi: 10.1101/2025.06.02.657148.
2
Evolutionary and Functional Analysis of Caspase-8 and ASC Interactions to Drive Lytic Cell Death, PANoptosis.半胱天冬酶-8与凋亡相关斑点样蛋白相互作用以驱动溶解性细胞死亡、PAN细胞凋亡的进化与功能分析
Mol Biol Evol. 2025 Apr 30;42(5). doi: 10.1093/molbev/msaf096.
3
Signalling by co-operative higher-order assembly formation: linking evidence at molecular and cellular levels.通过协同高阶组装形成进行信号传导：连接分子和细胞水平的证据
Biochem J. 2025 Mar 5;482(5):275-294. doi: 10.1042/BCJ20220094.
4
A structural atlas of death domain fold proteins reveals their versatile roles in biology and function.死亡结构域折叠蛋白的结构图谱揭示了它们在生物学和功能中的多种作用。
Proc Natl Acad Sci U S A. 2025 Feb 25;122(8):e2426986122. doi: 10.1073/pnas.2426986122. Epub 2025 Feb 20.
5
The Crosstalk of Apoptotic and Non-Apoptotic Signaling in CD95 System.CD95 系统中凋亡和非凋亡信号的串扰。
Cells. 2024 Nov 3;13(21):1814. doi: 10.3390/cells13211814.
6
The molecular evolution of cancer associated genes in mammals.癌症相关基因在哺乳动物中的分子进化。
Sci Rep. 2024 May 22;14(1):11650. doi: 10.1038/s41598-024-62425-0.
7
The Role of Cytokines in Cholesterol Accumulation in Cells and Atherosclerosis Progression.细胞因子在细胞胆固醇蓄积和动脉粥样硬化进展中的作用。
Int J Mol Sci. 2023 Mar 29;24(7):6426. doi: 10.3390/ijms24076426.
8
Protein supersaturation powers innate immune signaling.蛋白质过饱和增强先天性免疫信号传导。
bioRxiv. 2024 Mar 3:2023.03.20.533581. doi: 10.1101/2023.03.20.533581.
9
Structural Mechanisms of NLRP3 Inflammasome Assembly and Activation.NLRP3 炎性小体组装和激活的结构机制。
Annu Rev Immunol. 2023 Apr 26;41:301-316. doi: 10.1146/annurev-immunol-081022-021207. Epub 2023 Feb 7.
10
Rafting on the Plasma Membrane: Lipid Rafts in Signaling and Disease.在质膜上漂流：信号转导和疾病中的脂筏。
Adv Exp Med Biol. 2023;1436:87-108. doi: 10.1007/5584_2022_759.
本文引用的文献
1
Crystal structure of NALP3 protein pyrin domain (PYD) and its implications in inflammasome assembly.NALP3 蛋白的晶体结构 pyrin 域 (PYD) 及其在炎症小体组装中的意义。
J Biol Chem. 2011 Nov 11;286(45):39528-36. doi: 10.1074/jbc.M111.278812. Epub 2011 Aug 31.
2
The Fas-FADD death domain complex structure reveals the basis of DISC assembly and disease mutations.Fas-FADD 死亡结构域复合物的结构揭示了 DISC 组装和疾病突变的基础。
Nat Struct Mol Biol. 2010 Nov;17(11):1324-9. doi: 10.1038/nsmb.1920. Epub 2010 Oct 10.
3
Cutting edge: TCR ligation triggers digital activation of NF-kappaB.前沿：TCR 交联引发 NF-κB 的数字化激活。
J Immunol. 2010 Oct 15;185(8):4520-4. doi: 10.4049/jimmunol.1001051. Epub 2010 Sep 20.
4
Single-cell NF-kappaB dynamics reveal digital activation and analogue information processing.单细胞 NF-κB 动力学揭示了数字激活和模拟信息处理。
Nature. 2010 Jul 8;466(7303):267-71. doi: 10.1038/nature09145. Epub 2010 Jun 27.
5
Helical assembly in the MyD88-IRAK4-IRAK2 complex in TLR/IL-1R signalling.TLR/IL-1R 信号转导中 MyD88-IRAK4-IRAK2 复合物的螺旋组装。
Nature. 2010 Jun 17;465(7300):885-90. doi: 10.1038/nature09121. Epub 2010 May 19.
6
The inflammasomes.炎症小体。
Cell. 2010 Mar 19;140(6):821-32. doi: 10.1016/j.cell.2010.01.040.
7
An oligomeric signaling platform formed by the Toll-like receptor signal transducers MyD88 and IRAK-4.由Toll样受体信号转导分子MyD88和IRAK-4形成的寡聚信号平台。
J Biol Chem. 2009 Sep 11;284(37):25404-11. doi: 10.1074/jbc.M109.022392. Epub 2009 Jul 10.
8
Topology is the principal determinant in the folding of a complex all-alpha Greek key death domain from human FADD.拓扑结构是人类FADD中复杂的全α希腊钥匙死亡结构域折叠的主要决定因素。
J Mol Biol. 2009 Jun 5;389(2):425-37. doi: 10.1016/j.jmb.2009.04.004. Epub 2009 Apr 9.
9
The many roles of FAS receptor signaling in the immune system.FAS受体信号在免疫系统中的多种作用。
Immunity. 2009 Feb 20;30(2):180-92. doi: 10.1016/j.immuni.2009.01.001.
10
The interleukin-1 receptor/Toll-like receptor superfamily: 10 years of progress.白细胞介素-1受体/Toll样受体超家族：十年进展
Immunol Rev. 2008 Dec;226:10-8. doi: 10.1111/j.1600-065X.2008.00701.x.
Zotero 插件