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MST1/2 在炎症和免疫中的作用。

MST1/2 in inflammation and immunity.

机构信息

Department of Pulmonary and Critical Care Medicine, First Affiliated Hospital, Kunming Medical University, Kunming, China.

出版信息

Cell Adh Migr. 2023 Dec;17(1):1-15. doi: 10.1080/19336918.2023.2276616. Epub 2023 Nov 1.

DOI:10.1080/19336918.2023.2276616
PMID:37909712
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10761064/
Abstract

The mammalian Sterile 20-like kinase 1/2 (MST1/2) belongs to the serine/threonine (GC) protein kinase superfamily. Collective studies confirm the vital role MST1/2 in inflammation and immunity. MST1/2 is closely related to the progress of inflammation. Generally, MST1/2 aggravates the inflammatory injury through MST1-JNK, MST1-mROS, MST1-Foxo3, and NF-κB pathways, as well as several regulatory factors such as tumor necrosis factor-α (TNF-α), mitochondrial extension factor 1 (MIEF1), and lipopolysaccharide (LPS). Moreover, MST1/2 is also involved in the regulation of immunity to balance immune activation and tolerance by regulating MST1/2-Rac, MST1-Akt1/c-myc, MST1-Foxos, MST1-STAT, Btk pathways, and lymphocyte function-related antigen 1 (LFA-1), which subsequently prevents immunodeficiency syndrome and autoimmune diseases. This article reviews the effects of MST1/2 on inflammation and immunity.

摘要

哺乳动物无活性丝氨酸/苏氨酸激酶 1/2(MST1/2)属于丝氨酸/苏氨酸(GC)蛋白激酶超家族。大量研究证实 MST1/2 在炎症和免疫中起着至关重要的作用。MST1/2 与炎症的进展密切相关。通常情况下,MST1/2 通过 MST1-JNK、MST1-mROS、MST1-Foxo3 和 NF-κB 途径以及肿瘤坏死因子-α(TNF-α)、线粒体延伸因子 1(MIEF1)和脂多糖(LPS)等几种调节因子加重炎症损伤。此外,MST1/2 还参与免疫调节,通过调节 MST1/2-Rac、MST1-Akt1/c-myc、MST1-Foxos、MST1-STAT、Btk 途径和淋巴细胞功能相关抗原 1(LFA-1)来平衡免疫激活和耐受,从而防止免疫缺陷综合征和自身免疫性疾病。本文综述了 MST1/2 对炎症和免疫的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f2c/10761064/fe812fd83a17/KCAM_A_2276616_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f2c/10761064/2119a9932191/KCAM_A_2276616_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f2c/10761064/ca02c84dd524/KCAM_A_2276616_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f2c/10761064/c1abef500569/KCAM_A_2276616_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f2c/10761064/173a31344924/KCAM_A_2276616_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f2c/10761064/6ba49f0a16f0/KCAM_A_2276616_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f2c/10761064/fe812fd83a17/KCAM_A_2276616_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f2c/10761064/2119a9932191/KCAM_A_2276616_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f2c/10761064/ca02c84dd524/KCAM_A_2276616_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f2c/10761064/c1abef500569/KCAM_A_2276616_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f2c/10761064/173a31344924/KCAM_A_2276616_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f2c/10761064/6ba49f0a16f0/KCAM_A_2276616_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2f2c/10761064/fe812fd83a17/KCAM_A_2276616_F0006_OC.jpg

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