细胞质 HMGB2 在免疫细胞死亡过程中协调 CALR 转位。

IF 6.5 2区 医学 Q1 IMMUNOLOGY Oncoimmunology Pub Date : 2024-12-31 Epub Date: 2024-10-26 DOI:10.1080/2162402X.2024.2421028
Peng Liu, Liwei Zhao, Oliver Kepp, Guido Kroemer
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引用次数: 0

摘要

最近的一项体外研究表明,对核输出受体 XPO1 的药理抑制可抑制奥沙利铂诱导的 HMGB1 和 HMGB2 的核释放以及 CALR 向质膜的转位。此外,即使在没有奥沙利铂的情况下,细胞靶向 HMGB2 蛋白也能有效诱导 CALR 暴露。
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Cytoplasmic HMGB2 orchestrates CALR translocation in the course of immunogenic cell death.

A recent in vitro study showed that pharmacological inhibition of the nuclear export receptor XPO1 suppresses oxaliplatin-induced nuclear release of HMGB1 and HMGB2, as well as the translocation of CALR to the plasma membrane. Moreover, cell-targeted-HMGB2 protein potently induced CALR exposure, even in the absence of oxaliplatin.

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来源期刊
Oncoimmunology
Oncoimmunology ONCOLOGYIMMUNOLOGY-IMMUNOLOGY
CiteScore
12.50
自引率
2.80%
发文量
276
审稿时长
24 weeks
期刊介绍: OncoImmunology is a dynamic, high-profile, open access journal that comprehensively covers tumor immunology and immunotherapy. As cancer immunotherapy advances, OncoImmunology is committed to publishing top-tier research encompassing all facets of basic and applied tumor immunology. The journal covers a wide range of topics, including: -Basic and translational studies in immunology of both solid and hematological malignancies -Inflammation, innate and acquired immune responses against cancer -Mechanisms of cancer immunoediting and immune evasion -Modern immunotherapies, including immunomodulators, immune checkpoint inhibitors, T-cell, NK-cell, and macrophage engagers, and CAR T cells -Immunological effects of conventional anticancer therapies.
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