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SQSTM1/p62 抑制会损害缺氧人树突状细胞中的生存信号。

SQSTM1/p62 inhibition impairs pro-survival signaling in hypoxic human dendritic cells.

机构信息

Cellular and Molecular Physiology Unit, Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy.

Department of Medical Biotechnologies, University of Siena, Siena, Italy.

出版信息

Biochim Biophys Acta Mol Cell Res. 2024 Feb;1871(2):119625. doi: 10.1016/j.bbamcr.2023.119625. Epub 2023 Nov 18.

DOI:10.1016/j.bbamcr.2023.119625
PMID:37981035
Abstract

The sequestosome 1 (SQSTM1)/p62 is an adaptor protein which plays multiple roles in several cell functions, including cell survival and autophagy. Dendritic cells (DCs) are the most prominent antigen presenting cells and during their lifespan they are exposed to different oxygen tensions, including hypoxia. By using a siRNA approach we found out that p62 was implicated in the maintenance of Erk1/2 phosphorylation and preservation of hypoxic DC survival, as well as in the reduction of AMPK activation. Thus, p62 expression in DCs in hypoxic microenvironments, such as in the lymphoid organs, may extend their lifespan to ensure their functions.

摘要

自噬相关蛋白 SQSTM1/p62 作为衔接蛋白,在多种细胞功能中发挥重要作用,包括细胞存活和自噬。树突状细胞(DCs)是最突出的抗原提呈细胞,在其生命周期中,它们会暴露于不同的氧张力中,包括缺氧。通过 siRNA 方法,我们发现 p62 参与维持 Erk1/2 的磷酸化和维持缺氧 DC 的存活,以及减少 AMPK 的激活。因此,在缺氧微环境(如淋巴器官)中,DC 中的 p62 表达可能会延长其寿命,以确保其功能。

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