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生长抑制因子(ING)家族成员在健康与恶性肿瘤中的分子机制

Molecular mechanisms of inhibitor of growth (ING) family members in health and malignancy.

作者信息

Taheri Mohammad, Hussen Bashdar Mahmud, Najafi Sajad, Abak Atefe, Ghafouri-Fard Soudeh, Samsami Majid, Baniahmad Aria

机构信息

Institute of Human Genetics, Jena University Hospital, Jena, Germany.

Urology and Nephrology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

出版信息

Cancer Cell Int. 2022 Sep 2;22(1):272. doi: 10.1186/s12935-022-02693-w.

Abstract

ING genes belong to family of tumor suppressor genes with regulatory functions on cell proliferation, apoptosis, and cellular senescence. These include a family of proteins with 5 members (ING1-5), which are downregulated in human malignancies and/or affected by pathogenic mutations. ING proteins are highly evolutionarily conserved proteins containing several domains through which bind to chromatin structures by exerting their effects as readers of histone modification marks, and also binding to proteins like p53 involved in biological processes such as cell cycle regulation. Further, they are known as subunits of histone acetylation as well as deacetylation complexes and so exert their regulatory roles through epigenetic mechanisms. Playing role in restriction of proliferative but also invasive potentials of normal cells, INGs are particularly involved in cancer development and progression. However, additional studies and experimental confirmation are required for these models. This paper highlights the potential impact that INGs may have on the development of human cancer and explores what new information has recently arise on the functions of ING genes.

摘要

ING基因属于肿瘤抑制基因家族,对细胞增殖、凋亡和细胞衰老具有调节功能。这些基因包括一个由5个成员(ING1 - 5)组成的蛋白质家族,它们在人类恶性肿瘤中表达下调和/或受到致病突变的影响。ING蛋白是高度进化保守的蛋白质,包含几个结构域,通过作为组蛋白修饰标记的读取器发挥作用来与染色质结构结合,还能与参与细胞周期调控等生物过程的p53等蛋白质结合。此外,它们是组蛋白乙酰化和去乙酰化复合物的亚基,因此通过表观遗传机制发挥其调节作用。ING基因在限制正常细胞的增殖和侵袭潜能方面发挥作用,尤其参与癌症的发生和发展。然而,这些模型还需要更多的研究和实验证实。本文强调了ING基因可能对人类癌症发展产生的潜在影响,并探讨了ING基因功能方面最近出现的新信息。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff21/9438315/847ccadad589/12935_2022_2693_Fig1_HTML.jpg

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