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阴阳1:功能、机制与神经胶质细胞

Yin Yang 1: Function, Mechanisms, and Glia.

作者信息

Rodríguez-Campuzano Ada G, Castelán Francisco, Hernández-Kelly Luisa C, Felder-Schmittbuhl Marie-Paule, Ortega Arturo

机构信息

Departamento de Biología Celular y Fisiología, Unidad Foránea Tlaxcala, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Tlaxcala, Tlaxcala, Mexico.

Departamento de Toxicología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Av. IPN 2508, San Pedro Zacantenco, G.A. Madero, 07360, Ciudad de Mexico, Mexico.

出版信息

Neurochem Res. 2025 Feb 4;50(2):96. doi: 10.1007/s11064-025-04345-7.

Abstract

Yin Yang 1 is a ubiquitously expressed transcription factor that has been extensively studied given its particular dual transcriptional regulation. Yin Yang 1 is involved in various cellular processes like cell cycle progression, cell differentiation, DNA repair, cell survival and apoptosis among others. Its malfunction or alteration leads to disease and even to malignant transformation. This transcription factor is essential for the proper central nervous system development and function. The activity of Yin Yang 1 depends on its interacting partners, promoter environment and chromatin structure, however, its mechanistic activity is not completely understood. In this review, we briefly discuss the Yin Yang 1 structure, post-translational modifications, interactions, mechanistic functions and its participation in neurodevelopment. We also discuss its expression and critical involvement in the physiology and physiopathology of glial cells, summarizing the contribution of Yin Yang 1 on different aspects of cellular function.

摘要

阴阳1是一种广泛表达的转录因子,鉴于其特殊的双重转录调控作用,已得到广泛研究。阴阳1参与多种细胞过程,如细胞周期进程、细胞分化、DNA修复、细胞存活和凋亡等。其功能失调或改变会导致疾病,甚至恶性转化。这种转录因子对中枢神经系统的正常发育和功能至关重要。阴阳1的活性取决于其相互作用的伙伴、启动子环境和染色质结构,然而,其作用机制尚未完全明确。在本综述中,我们简要讨论阴阳1的结构、翻译后修饰、相互作用、作用机制及其在神经发育中的作用。我们还讨论了其在神经胶质细胞生理和病理生理中的表达及关键作用,总结了阴阳1在细胞功能不同方面的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bfd4/11794380/f18d7e58f398/11064_2025_4345_Fig1_HTML.jpg

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