The structure and function of multifunctional protein ErbB3 binding protein 1 (Ebp1) and its role in diseases

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Cell Biology International Pub Date : 2024-06-17 DOI:10.1002/cbin.12196

Ying Wang, Jianxiao Xing, Yanyang Liang, Huifang Liang, Nannan Liang, Junqin Li, Guohua Yin, Xinhua Li, Kaiming Zhang

引用次数: 0

Abstract

ErbB3-binding protein 1(Ebp1) has two isoforms, p42 Ebp1 and p48 Ebp1, both of which can regulate cell growth and differentiation. But these isoforms often have opposite effects, including contradictory roles in regulation of cell growth in different tissues and cells. P48 Ebp1 belongs to the full-length sequence, while conformational changes in the crystal structure of p42 Ebp1 reveals a lack of an α helix at the amino terminus. Due to the differences in the structures of these two isoforms, they have different binding partners and protein modifications. Ebp1 can function as both an oncogene and a tumor suppressor factor. However, the underlying mechanisms by which these two isoforms exert opposite functions are still not fully understood. In this review, we summarize the genes and the structures of protein of these two isoforms, protein modifications, binding partners and the association of different isoforms with diseases.

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多功能蛋白 ErbB3 结合蛋白 1（Ebp1）的结构和功能及其在疾病中的作用。

ErbB3结合蛋白1（Ebp1）有两种异构体，即p42 Ebp1和p48 Ebp1，它们都能调节细胞的生长和分化。但这两种异构体往往具有相反的作用，包括在不同组织和细胞中调控细胞生长的矛盾作用。P48 Ebp1 属于全长序列，而 p42 Ebp1 晶体结构的构象变化显示其氨基末端缺少一个 α 螺旋。由于这两种异构体的结构不同，它们的结合伙伴和蛋白质修饰也不同。Ebp1 既可作为致癌基因，也可作为肿瘤抑制因子。然而，这两种异构体发挥相反功能的内在机制仍未完全明了。在这篇综述中，我们总结了这两种异构体的基因和蛋白结构、蛋白修饰、结合伙伴以及不同异构体与疾病的关联。

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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来源期刊

Cell Biology International 生物-细胞生物学

CiteScore

7.60

自引率

0.00%

发文量

208

审稿时长

1 months

期刊介绍： Each month, the journal publishes easy-to-assimilate, up-to-the minute reports of experimental findings by researchers using a wide range of the latest techniques. Promoting the aims of cell biologists worldwide, papers reporting on structure and function - especially where they relate to the physiology of the whole cell - are strongly encouraged. Molecular biology is welcome, as long as articles report findings that are seen in the wider context of cell biology. In covering all areas of the cell, the journal is both appealing and accessible to a broad audience. Authors whose papers do not appeal to cell biologists in general because their topic is too specialized (e.g. infectious microbes, protozoology) are recommended to send them to more relevant journals. Papers reporting whole animal studies or work more suited to a medical journal, e.g. histopathological studies or clinical immunology, are unlikely to be accepted, unless they are fully focused on some important cellular aspect. These last remarks extend particularly to papers on cancer. Unless firmly based on some deeper cellular or molecular biological principle, papers that are highly specialized in this field, with limited appeal to cell biologists at large, should be directed towards journals devoted to cancer, there being very many from which to choose.