表观遗传调控的神秘性：人类非编码 RNA nc886 的非凡案例。

IF 3 4区医学 Q2 GENETICS & HEREDITY

Epigenomics Pub Date : 2024-10-28 DOI:10.1080/17501911.2024.2415278

Yeon-Su Lee, Yong Sun Lee

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引用次数: 0

摘要

nc886 是一种调控性非编码 RNA，由 RNA 聚合酶 III（Pol III）转录，在不同的生物环境中表达各异，并在炎症和癌症中发挥作用。表观遗传机制在调控 nc886 表达方面发挥着令人好奇的作用。nc866 作为一个母系印记基因和可转移的外显子，表现出多态性印记，其甲基化状态受环境和生物因素的影响。因此，nc886 启动子 DNA 甲基化状态以及由此产生的不同 RNA 表达水平与生理和病理状况相关。在这篇综述中，我们总结了相关文献，并探讨了与 nc886 不同作用相关的意义。

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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The mystique of epigenetic regulation: the remarkable case of a human noncoding RNA, nc886.

nc886 is a regulatory noncoding RNA that is transcribed by RNA polymerase III (Pol III), is variably expressed in different biological contexts, and plays roles in inflammation and cancer. Epigenetic mechanisms play an intriguing role in regulating nc886 expression. As a maternally imprinted gene and metastable epiallele, nc866 exhibits polymorphic imprinting, with a methylation status that is influenced by environmental and biological factors. Consequently, the promoter DNA methylation status and the different resulting RNA expression levels of nc886 are associated with physiological and pathological conditions. In this review, we summarize the literature and explore the significance in relation to diverse roles of nc886.

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来源期刊

Epigenomics GENETICS & HEREDITY-

CiteScore

5.80

自引率

2.60%

发文量

审稿时长

>12 weeks

期刊介绍： Epigenomics provides the forum to address the rapidly progressing research developments in this ever-expanding field; to report on the major challenges ahead and critical advances that are propelling the science forward. The journal delivers this information in concise, at-a-glance article formats – invaluable to a time constrained community. Substantial developments in our current knowledge and understanding of genomics and epigenetics are constantly being made, yet this field is still in its infancy. Epigenomics provides a critical overview of the latest and most significant advances as they unfold and explores their potential application in the clinical setting.