X-chromosome-linked inhibitor of apoptosis protein (XIAP) controls cell survival in several regulated cell death pathways and coordinates a range of inflammatory signaling events. Initially identified as a caspase-binding protein, it was considered to be primarily involved in blocking apoptosis from both intrinsic as well as extrinsic triggers. However, XIAP also prevents TNF-mediated, receptor-interacting protein 3 (RIPK3)-dependent cell death, by controlling RIPK1 ubiquitylation and preventing inflammatory cell death. The identification of patients with germline mutations in XIAP (termed XLP-2 syndrome) pointed toward its role in inflammatory signaling. Indeed, XIAP also mediates nucleotide-binding oligomerization domain-containing 2 (NOD2) proinflammatory signaling by promoting RIPK2 ubiquitination within the NOD2 signaling complex leading to NF-κB and MAPK activation and production of inflammatory cytokines and chemokines. Overall, XIAP is a critical regulator of multiple cell death and inflammatory pathways making it an attractive drug target in tumors and inflammatory diseases.

中文翻译：

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XIAP 对细胞死亡和免疫的调节。

X 染色体相关的凋亡蛋白抑制剂 (XIAP) 在几种受调节的细胞死亡途径中控制细胞存活，并协调一系列炎症信号事件。最初被鉴定为半胱天冬酶结合蛋白，它被认为主要参与阻断内在和外在触发因素的细胞凋亡。然而，XIAP 还通过控制 RIPK1 泛素化和防止炎症性细胞死亡来防止 TNF 介导的受体相互作用蛋白 3 (RIPK3) 依赖性细胞死亡。XIAP（称为 XLP-2 综合征）中具有种系突变的患者的鉴定表明其在炎症信号传导中的作用。的确，XIAP 还通过促进 NOD2 信号复合物内的 RIPK2 泛素化来介导含有核苷酸结合寡聚化结构域 2 (NOD2) 的促炎信号传导，从而导致 NF-κB 和 MAPK 激活以及炎性细胞因子和趋化因子的产生。总体而言，XIAP 是多种细胞死亡和炎症通路的关键调节剂，使其成为肿瘤和炎症性疾病中有吸引力的药物靶点。