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

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。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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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 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.