Ripk1 and haematopoiesis: a case for LUBAC and Ripk3.
Ripk1 and haematopoiesis: a case for LUBAC and Ripk3.
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DOI：
10.1038/s41418-018-0135-2
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发表时间：
2018-08
影响因子：
12.4
通讯作者：
Meier P
中科院分区：
文献类型：
--
作者：
Annibaldi A;Meier P
虽然长期以来被认为是炎症组织的一个组成部分，但细胞死亡作为一种有助于组织稳态、炎症和疾病发病机制的活性成分的潜在作用最近才得到关注[1]。细胞死亡组分与炎症信号传导途径硬连线的概念表明，这些死亡组分充当组织稳态的正调节剂，增强上皮细胞对组织应激的恢复力[1，2]专用传感器已经发展成检测不同的应激源并诱导适应性反应。受体相互作用丝氨酸/苏氨酸蛋白激酶1（Ripk 1）代表了这种传感器，在调节对组织应激的适应性反应中起信号传导节点的作用[1]。Ripk 1在各种输入信号之后被激活，例如响应于肿瘤坏死因子（TNF）家族细胞因子、模式识别受体和干扰素。Ripk 1可以激活丝裂原活化蛋白激酶、核因子κB（NF-κB）和凋亡以及坏死性细胞死亡[1]。Ripk 1以激酶依赖性和/或支架依赖性方式介导这些作用。虽然Ripk 1的支架功能维持组织稳态[1]，但Ripk 1的激酶活性是坏死性凋亡所必需的，并且取决于细胞背景，细胞凋亡[3，4]。Ripk 1受到泛素化、磷酸化和半胱天冬酶介导的切割的严格控制[1，5，6]。过多或过少的Ripk 1活性都可能导致细胞死亡、慢性炎症和致命性。了解Ripk 1是如何调节的对正常发育和疾病病理学（如慢性炎症和癌症）具有重要意义。但它也为免疫肿瘤学提供了新的机会，因为Ripk 1和NF-κB信号传导是CD 8 + T细胞的抗原交叉致敏所必需的[7]。
Although long recognized as a component of inflamed tissues, the potential role of cell death as an active component that contributes to tissue homeostasis, inflammation and disease pathogenesis has only recently gained attention [1]. The notion that cell death components are hard-wired into inflammatory signaling pathways indicates that such death components act as positive regulators of tissue homeostasis, enhancing the resilience of epithelia to tissue stress [1, 2] Dedicated sensors have evolved to detect different stressors and induce adaptive responses. Receptorinteracting serine/threonine-protein kinase 1 (Ripk1) represents such sensor, functioning as signaling node in regulating adaptive responses to tissue stress [1]. Ripk1 is activated following a variety of input signals, such as in response to tumor necrosis factor (TNF) family cytokines, pattern recognition receptors and interferons. Ripk1 can activate mitogen-activated protein kinases, nuclear factorκB (NF-κB) and apoptotic as well as necrotic cell death [1].Ripk1 mediates these effects in a kinase-dependent and/or scaffold-dependent manner. While the scaffold function of Ripk1 maintains tissue homeostasis [1], the kinase activity of Ripk1 is required for necroptosis, and, depending on the cellular context, apoptosis [3, 4]. Ripk1 is tightly controlled by ubiquitylation, phosphorylation and caspase-mediated cleavage [1, 5, 6]. Too much or too little Ripk1 activity can lead to cell death, chronic inflammation and lethality. Understanding how Ripk1 is regulated has important implications for normal development and disease pathologies, such as chronic inflammation and cancer. But it also offers novel opportunities for immuno-oncology as Ripk1 and NF-κB signaling is required for antigen cross-priming of CD8+ T cells [7].
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影响因子：
16
作者：
Annibaldi A;Wicky John S;Vanden Berghe T;Swatek KN;Ruan J;Liccardi G;Bianchi K;Elliott PR;Choi SM;Van Coillie S;Bertin J;Wu H;Komander D;Vandenabeele P;Silke J;Meier P
通讯作者：
Meier P
影响因子：
9
作者：
Geserick P;Wang J;Schilling R;Horn S;Harris PA;Bertin J;Gough PJ;Feoktistova M;Leverkus M
通讯作者：
Leverkus M
DOI：
10.4049/jimmunol.1400499
发表时间：
2014-06-15
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Berger SB;Kasparcova V;Hoffman S;Swift B;Dare L;Schaeffer M;Capriotti C;Cook M;Finger J;Hughes-Earle A;Harris PA;Kaiser WJ;Mocarski ES;Bertin J;Gough PJ
通讯作者：
Gough PJ
影响因子：
16
作者：
Jaco I;Annibaldi A;Lalaoui N;Wilson R;Tenev T;Laurien L;Kim C;Jamal K;Wicky John S;Liccardi G;Chau D;Murphy JM;Brumatti G;Feltham R;Pasparakis M;Silke J;Meier P
通讯作者：
Meier P
影响因子：
8.8
作者：
Peltzer, Nieves;Rieser, Eva;Walczak, Henning
通讯作者：
Walczak, Henning