VII. Are lymphomas driven by epigenetic lesions?
VII. Are lymphomas driven by epigenetic lesions?
复制标题
七．
DOI：
10.1002/hon.2215
复制
发表时间：
2015
影响因子：
3.3
通讯作者：
Melnick,AriM
中科院分区：
文献类型：
--
作者：
Boss,IsaacW;Melnick,AriM
Epigenetic regulation of gene expression is a process driven by dynamic changes in chromatin architecture carried out by histone-modifying enzymes. In eukaryotic organisms, chromatin organization allows tight packaging of the genome while still allowing access to transcriptional machinery. The basic unit of chromatin is the nucleosome, which consists of DNA wrapped around an octamer of histone proteins. Histone tails are post-translationally modified by covalent modifications such as methylation or acetylation that occur at lysine and arginine residues. These histone modifications, or ‘marks’, result in changes to chromatin structure and serve as a histone code that directs the ordered recruitment of effector proteins that control gene transcription, replication and DNA repair [1]. A number of enzymes are responsible for establishing the histone code, by functioning as writers, readers and erasers of histone marks. These epigenetic modifiers are directed by transcription factors to histones located within DNA regulatory elements, including enhancers and promoters, allowing gene expression to be turned on or off. Histone marks associated with transcriptional activation include histone 3 lysine 4 methylation (H3K4me) and H3 lysine 27 acetylation (H3K27ac), whereas H3 lysine 27 methylation (H3K27me) is generally linked to repression. The functional state of enhancer regions that control cell context-specific gene expression can be defined from the chromatin standpoint as being in an active (H3K4me1/2 and H3K27ac), or poised (H3K4me1/2 and H3K27me3) configuration. Specific patterning of histone marks is context dependent and can change rapidly in response to external stimuli, providing a layer of epigenetic control to regulate cell fate and function decisions. Somatic mutation of histone-modifying enzymes is now recognized as a hallmark of certain forms of B-cell lymphomas. Here, we will focus on some of the more frequently affected histone-modifying enzymes in B-cell lymphomas and their potential mechanisms of action.
登录
查看更多内容
灵长类动物动脉粥样硬化和高血压中的动脉溶酶体和结缔组织。
影响因子：
20.1
作者：
H. Wolinsky;S. Goldfischer;M. M. Daly;L. Kasak;B. Coltoff
通讯作者：
B. Coltoff
泡沫细胞和动脉粥样硬化形成
影响因子：
5.2
作者：
S. D. Fowler;E. Mayer;P. Greenspan
通讯作者：
P. Greenspan
早期动脉粥样硬化中同时存在内皮细胞更新和白细胞边缘化。
DOI：
--
发表时间：
1983
期刊：
Scanning electron microscopy
影响因子：
--
作者：
Jerome,WG;Lewis,JC;Taylor,RG;White,MS
通讯作者：
White,MS
动脉粥样硬化的病理学。
影响因子：
6.7
作者：
Neville Woolf;Alan T. Marty
通讯作者：
Alan T. Marty
DOI：
--
发表时间：
1983-12
期刊：
The American journal of pathology
影响因子：
--
作者：
I. Joris;T. Zand;J. Nunnari;F. Krolikowski;G. Majno
通讯作者：
I. Joris;T. Zand;J. Nunnari;F. Krolikowski;G. Majno