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半乳糖凝集素-3 对 T 细胞激活的调节:膜重塑的机制。

Galectin-3 modulation of T-cell activation: mechanisms of membrane remodelling.

机构信息

EMBL Australia Node in Single Molecule Science, University of New South Wales, Sydney 2052, Australia; ARC Centre of Excellence in Advanced Molecular Imaging, University of New South Wales, Sydney 2052, Australia.

Institut Curie, PSL Research University, Cellular and Chemical Biology unit, UMR3666, CNRS, U1143, INSERM, 26 rue d'Ulm, 75248 Paris Cedex 05, France.

出版信息

Prog Lipid Res. 2019 Oct;76:101010. doi: 10.1016/j.plipres.2019.101010. Epub 2019 Nov 1.

Abstract

Galectin-3 (Gal3) is a multifaceted protein which belongs to a family of lectins and binds β-galactosides. Gal3 expression is altered in many types of cancer, with increased expression generally associated with poor prognosis. Although the mechanisms remain unknown, Gal3 has been implicated in several biological processes involved in cancer progression, including suppression of T cell-mediated immune responses. Extracellular Gal3 binding to the plasma membrane of T cells alters membrane organization and the formation of an immunological synapse. Its multivalent capacity allows Gal3 to interact specifically with different membrane proteins and lipids, influencing endocytosis, trafficking and T cell receptor signalling. The ability of Gal3 to inhibit T cell responses may provide a mechanism by which Gal3 aids in cancer progression. In this review, we seek to give an overview of the mechanisms by which Gal3 alters the spatial organization of cell membranes and how these processes impact on T cell activation.

摘要

半乳糖凝集素 3(Gal3)是一种多功能蛋白,属于凝集素家族,能与β-半乳糖苷结合。Gal3 在多种类型的癌症中表达发生改变,通常表达增加与预后不良有关。尽管其机制尚不清楚,但 Gal3 已被牵涉到涉及癌症进展的几个生物学过程中,包括抑制 T 细胞介导的免疫反应。细胞外 Gal3 与 T 细胞的质膜结合会改变膜组织和免疫突触的形成。其多价能力使 Gal3 能够与不同的膜蛋白和脂质特异性相互作用,影响内吞作用、运输和 T 细胞受体信号转导。Gal3 抑制 T 细胞反应的能力可能为 Gal3 促进癌症进展提供了一种机制。在这篇综述中,我们试图概述 Gal3 改变细胞膜空间组织的机制,以及这些过程如何影响 T 细胞的激活。

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