UTX 基因突变与人类癌症。
UTX Mutations in Human Cancer.
机构信息
Simpson Querrey Center for Epigenetics, Department of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Searle 6-512, 320 E. Superior St., Chicago, IL 60611, USA.
Simpson Querrey Center for Epigenetics, Department of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Searle 6-512, 320 E. Superior St., Chicago, IL 60611, USA.
出版信息
Cancer Cell. 2019 Feb 11;35(2):168-176. doi: 10.1016/j.ccell.2019.01.001.
Ubiquitously transcribed tetratricopeptide repeat on chromosome X (UTX, encoded by KDM6A) is a histone demethylase that targets di- and tri-methylated histone H3 lysine 27 (H3K27). UTX function has been linked to homeotic gene expression, embryonic development, and cellular reprogramming. UTX and its protein interactors within the COMPASS family, including the MLL3 and MLL4 lysine methyltransferases, are frequently mutated in multiple human cancers; however, the molecular basis of how these mutations contribute to oncogenesis remains unclear. Here, we discuss catalytic-dependent and -independent functions of UTX and its partners MLL3 and MLL4 as part of the COMPASS family during development and in oncogenesis.
X 染色体上普遍转录的四肽重复蛋白（UTX，由 KDM6A 编码）是一种组蛋白去甲基化酶，靶向二甲基化和三甲基化的组蛋白 H3 赖氨酸 27（H3K27）。UTX 的功能与同源盒基因表达、胚胎发育和细胞重编程有关。UTX 及其在 COMPASS 家族中的蛋白相互作用物，包括 MLL3 和 MLL4 赖氨酸甲基转移酶，在多种人类癌症中经常发生突变；然而，这些突变如何促进肿瘤发生的分子基础尚不清楚。在这里，我们讨论了 UTX 及其伙伴 MLL3 和 MLL4 在发育和致癌过程中作为 COMPASS 家族的一部分的催化依赖和非依赖功能。
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