An Update on CARD Only Proteins (COPs) and PYD Only Proteins (POPs) as Inflammasome Regulators.
An Update on CARD Only Proteins (COPs) and PYD Only Proteins (POPs) as Inflammasome Regulators.
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DOI：
10.3390/ijms21186901
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发表时间：
2020-09-20
影响因子：
5.6
通讯作者：
Dorfleutner A
中科院分区：
文献类型：
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作者：
Devi S;Stehlik C;Dorfleutner A
炎性小体是激活caspase-1和随后释放白介素1β、IL-18和危险信号所需的蛋白质支架，以及在感染和无菌组织损伤后诱导嗜酸性细胞死亡以恢复体内平衡所需的蛋白质支架。然而，过度的炎性小体激活也会导致有害的炎症性疾病。因此，广泛的控制机制是必要的，以防止不当的炎症体反应和炎症性疾病。炎性小体是由含有吡咯结构域(PYD)和半胱氨酸酶招募结构域(CARD)的炎性小体组成的有序成核聚合而成的。一旦聚合成核，这个过程就会以一种自我延续的方式进行，并代表着一个不可逆转的点。因此，调控这一关键步骤对于受控的炎症体反应至关重要。在这里，我们提供了包含PYD或CARD的两个单域蛋白家族的最新进展，分别是PYD-Only Proteins(POPS)和CardOnly Proteins(COPS)。它们的结构允许它们占据并阻止炎性小体组装所需的关键蛋白质-蛋白质相互作用域的访问，从而调节这些有核聚合事件的阈值，从而调节炎症宿主反应。
Inflammasomes are protein scaffolds required for the activation of caspase-1 and the subsequent release of interleukin (IL)-1β, IL-18, and danger signals, as well as the induction of pyroptotic cell death to restore homeostasis following infection and sterile tissue damage. However, excessive inflammasome activation also causes detrimental inflammatory disease. Therefore, extensive control mechanisms are necessary to prevent improper inflammasome responses and inflammatory disease. Inflammasomes are assembled by sequential nucleated polymerization of Pyrin domain (PYD) and caspase recruitment domain (CARD)-containing inflammasome components. Once polymerization is nucleated, this process proceeds in a self-perpetuating manner and represents a point of no return. Therefore, regulation of this key step is crucial for a controlled inflammasome response. Here, we provide an update on two single domain protein families containing either a PYD or a CARD, the PYD-only proteins (POPs) and CARD-only proteins (COPs), respectively. Their structure allows them to occupy and block access to key protein–protein interaction domains necessary for inflammasome assembly, thereby regulating the threshold of these nucleated polymerization events, and consequently, the inflammatory host response.
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朊病毒样聚合是抗病毒免疫防御和炎症小体激活中信号转导的基础。
影响因子：
64.5
作者：
Cai X;Chen J;Xu H;Liu S;Jiang QX;Halfmann R;Chen ZJ
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DOI：
10.4049/jimmunol.0802367
发表时间：
2009-03-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
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影响因子：
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作者：
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DOI：
10.1073/pnas.1607769113
发表时间：
2016-07-12
影响因子：
11.1
作者：
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通讯作者：
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影响因子：
30.5
作者：
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