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[1]阎 晗,于明航 综 述,尹 洁,等.组蛋白H3K4甲基转移酶KMT2D研究进展[J].天津医科大学学报,2018,24(06):562-565.
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组蛋白H3K4甲基转移酶KMT2D研究进展(PDF)
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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
24卷
期数:
2018年06期
页码:
562-565
栏目:
综述
出版日期:
2018-11-20

文章信息/Info

Title:
-
作者:
阎 晗于明航 综 述 尹 洁王 玺 审 校
(天津医科大学细胞生物学系,天津 300070)
Author(s):
-
关键词:
KMT2DH3K4甲基转移酶H3K4甲基化增强子表观遗传调控
Keywords:
-
分类号:
Q7
DOI:
-
文献标志码:
A
摘要:
组蛋白-赖氨酸 N-甲基转移酶2D(KMT2D),属于哺乳动物H3K4甲基转移酶家族成员,在成人组织中广泛表达,对于早期胚胎发育有重要作用。C-末端的SET区域负责组蛋白H3K4甲基化,维持KMT2D蛋白的稳定性。KMT2D与WRAD、NCOA6、PTIP、PA1和H3K27去甲基化酶 UTX组成复合物,在其中起到支架蛋白的作用,维持UTX的稳定性。KMT2D主要催化哺乳动物H3K4单甲基化,与转录因子共同作用于增强子区域,从而调控基因表达。KMT2D在调节细胞发育、分化、新陈代谢和肿瘤抑制方面具有重要作用,其突变导致多种疾病发生。进一步研究KMT2D有助于揭示其异常所引发多种疾病的病因,并且对开发临床药物提供有力的帮助。
Abstract:
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参考文献/References:


[1] Calo E,Wysocka J. Modification of enhancer chromatin: what,how,and why? [J]. Mol Cell,2013,49(5): 825
[2] Roguev A,Schaft D,Shevchenko A,et al. The saccharomyces cerevisiae set1 complex includes an Ash2 homologue and methylates histone 3 lysine 4 [J]. EMBO J,2001,20(24): 7137
[3] Ruthenburg A J,Allis C D,Wysocka J. Methylation of lysine 4 on histone H3: intricacy of writing and reading a single epigenetic mark [J]. Mol Cell,2007,25(1): 15
[4] Dhar S S,Lee S H,Kan P Y,et al. Trans-tail regulation of MLL4-catalyzed H3K4 methylation by H4R3 symmetric dimethylation is mediated by a tandem PHD of MLL4 [J]. Gene Dev,2012,26(24): 2749
[5] Dorighi K M,Swigut T,Henriques T,et al. Mll3 and Mll4 Facilitate Enhancer RNA Synthesis and Transcription from Promoters Independently of H3K4 Monomethylation [J]. Mol Cell,2017,66(4):568
[6] Jang Y,Wang C,Zhuanng L,et al. H3K4 Methyltransferase Activity Is Required for MLL4 Protein Stability[J]. J Mol Biol,2017, 429(13): 2046
[7] Rao R C,Dou Y. Hijacked in cancer: the KMT2 (MLL) family of methyltransferases [J]. Nat Rev Cancer,2015,15(6): 334
[8] Cho Y W,Hong T,Hong S,et al. PTIP associates with MLL3- and MLL4-containing histone H3 lysine 4 methyltransferase complex [J]. J Biol Chem,2007,282(28): 20395
[9] Lee M G,Villa R,Trojer P,et al. Demethylation of H3K27 regulates polycomb recruitment and H2A ubiquitination[J]. Science,2007, 318(5849): 447
[10] Erns T P,Vakoc C R. WRAD: enabler of the SET1-family of H3K4 methyltransferases [J]. Brief Funct Genomics,2012,11(3): 217
[11] Cho Y W,Hong S,Ge K. Affinity purification of MLL3/MLL4 histone H3K4 methyltransferase complex[J]. Methods Mol Biol,2012, 809: 465
[12] Bulger M,Groudine M. Functional and mechanistic diversity of distal transcription enhancers [J]. Cell,2011,144(3): 327
[13] Lee J E,Wang C,Xu S,et al. H3K4 mono-and di-methyltransferase MLL4 is required for enhancer activation during cell differentiation [J]. Elife,2013,2: e01503
[14] Lai B,Lee J E,Jang Y,et al. MLL3/MLL4 are required for CBP/p300 binding on enhancers and super-enhancer formation in brown adipogenesis [J]. Nucleic Acids Res,2017,45(11): 6388
[15] Wang C,Lee J E,Lai B,et al. Enhancer priming by H3K4 methyltransferase MLL4 controls cell fate transition[J]. P Natl Acad Sci USA,2016,113(42): 11871
[16] Faralli H,Wang C,Nakka K,et al. UTX demethylase activity is required for satellite cell-mediated muscle regeneration[J]. J Clin Invest,2016,126(4): 1555
[17] Ang S Y,Uebersohm A,Spencer C I,et al. KMT2D regulates specific programs in heart development via histone H3 lysine 4 di-methylation [J]. Development,2016,143(5): 810
[18] Ortega-molina A,Boss I W,Canfla A,et al. The histone lysine methyltransferase KMT2D sustains a gene expression program that represses B cell lymphoma development[J]. Nat Med,2015,21(10): 1199
[19] Munehira Y,Yang Z,Gozani O. Systematic analysis of known and candidate lysine demethylases in the regulation of myoblast differentiation [J]. J Mol Biol,2017,429(13): 2055
[20] Kim D H,Rhee J C,Yeo S,et al. Crucial roles of mixed-lineage leukemia 3 and 4 as epigenetic switches of the hepatic circadian clock controlling bile acid homeostasis in mice[J]. Hepatology,2015, 61(3): 1012
[21] Kim D H,Kim J,Kwon J S,et al. Critical roles of the histone methyltransferase MLL4/KMT2D in murine hepatic steatosis directed by ABL1 and PPARgamma2[J]. Cell Rep,2016,17(6): 1671v
[22] Lee J,Kim D H,Lee S,et al. A tumor suppressive coactivator complex of p53 containing ASC-2 and histone H3-lysine-4 methyltransferase MLL3 or its paralogue MLL4 [J]. P Natl Acad Sci USA,2009,106(21): 8513b
[23] Chen C,Liu Y,Rappaport A R,et al. MLL3 is a haploinsufficient 7q tumor suppressor in acute myeloid leukemia[J]. Cancer Cell,2014, 25(5): 652
[24] Zhang J,Dominguez-sola D,Hussein S,et al. Disruption of KMT2D perturbs germinal center B cell development and promotes lymphomagenesis [J]. Nat Med,2015,21(10): 1190
[25] Guo C,Chen L H,Huang Y,et al. KMT2D maintains neoplastic cell proliferation and global histone H3 lysine 4 monomethylation[J]. Oncotarget,2013,4(11): 2144
[26] Kim J H,Sharma A,Dhar S S,et al. UTX and MLL4 coordinately regulate transcriptional programs for cell proliferation and invasiveness in breast cancer cells[J]. Cancer Res,2014,74(6): 1705
[27] Toska E,Osmabeyoglu H U,Castel P,et al. PI3K pathway regulates ER-dependent transcription in breast cancer through the epigenetic regulator KMT2D [J]. Science,2017,355(6331): 1324
[28] BogershauSsen N,Wollnik B. Unmasking Kabuki syndrome [J]. Clin Genet,2013,83(3): 201
[29] Zaidl S,Choi M,Wakimoto H,et al. De novo mutations in histone-modifying genes in congenital heart disease[J]. Nature,2013,498(7453): 220
[30] Lawrence M S,Stojanov P,Mermel C H,et al. Discovery and saturation analysis of cancer genes across 21 tumour types[J]. Nature,2014,505(7484): 495
[31] Jones D T,Jager N,Kool M,et al. Dissecting the genomic complexity underlying medulloblastoma [J]. Nature,2012,488(7409): 100
[32] Juhlin C C,Stenman A,Haglund F,et al. Whole-exome sequencing defines the mutational landscape of pheochromocytoma and identifies KMT2D as a recurrently mutated gene[J]. Genes Chromosomes Cancer,2015,54(9): 542
[33] Morin R D,Mendez-Lago M,Mungall A J,et al. Frequent mutation of histone-modifying genes in non-Hodgkin lymphoma [J]. Nature,2011,476(7360): 298
[34] Lohr J G,Stojanov P,Lawrence M S,et al. Discovery and prioritization of somatic mutations in diffuse large B-cell lymphoma (DLBCL) by whole-exome sequencing[J]. P Natl Acad Sci USA,2012,109(10): 3879
[35] Gao Y B,Chen Z L,Li J G,et al. Genetic landscape of esophageal squamous cell carcinoma [J]. Nat Genet,2014,46(10): 1097
[36] Sausen M,Phallen J,Adleff V,et al. Clinical implications of genomic alterations in the tumour and circulation of pancreatic cancer patients [J]. Nat Commun,2015,6: 7686
[37] Grasso C S,Wu Y M,Robinson D R,et al. The mutational landscape of lethal castration-resistant prostate cancer[J]. Nature,2012,487(7406): 239

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备注/Memo

备注/Memo:
基金项目 国家重点基础研究发展计划基金资助项目(2014CB910100);国家自然科学基金资助项目(31600705);国家自然科学基金资助项目(31600693)
作者简介 阎晗(1989-),女,助理实验师,硕士,研究方向:肿瘤免疫;通信作者:王玺,E-mail:wangxi@tmu.edu.cn。
更新日期/Last Update: 2018-11-30