Noncoding RNA regulation of myeloid transcription factors, DNA methylation, and leukemia

2015 ◽  
Vol 43 (9) ◽  
pp. S27
Author(s):  
Daniel G. Tenen
Genes ◽  
2021 ◽  
Vol 12 (5) ◽  
pp. 759
Author(s):  
Zhongjing Su ◽  
Guangyu Liu ◽  
Bin Zhang ◽  
Ze Lin ◽  
Dongyang Huang

The leukocyte common antigen CD45 is a transmembrane phosphatase expressed on all nucleated hemopoietic cells, and the expression levels of its splicing isoforms are closely related to the development and function of lymphocytes. PEBP1P3 is a natural antisense transcript from the opposite strand of CD45 intron 2 and is predicted to be a noncoding RNA. The genotype-tissue expression and quantitative PCR data suggested that PEBP1P3 might be involved in the regulation of expression of CD45 splicing isoforms. To explore the regulatory mechanism of PEBP1P3 in CD45 expression, DNA methylation and histone modification were detected by bisulfate sequencing PCR and chromatin immunoprecipitation assays, respectively. The results showed that after the antisense RNA PEBP1P3 was knocked down by RNA interference, the DNA methylation of CD45 intron 2 was decreased and histone H3K9 and H3K36 trimethylation at the alternative splicing exons of CD45 DNA was increased. Knockdown of PEBP1P3 also increased the binding levels of chromatin conformation organizer CTCF at intron 2 and the alternative splicing exons of CD45. The present results indicate that the natural antisense RNA PEBP1P3 regulated the alternative splicing of CD45 RNA, and that might be correlated with the regulation of histone modification and DNA methylation.


2016 ◽  
Vol 68 (8) ◽  
pp. 1876-1886 ◽  
Author(s):  
Oscar Alvarez-Garcia ◽  
Kathleen M. Fisch ◽  
Nathan E. Wineinger ◽  
Ryuichiro Akagi ◽  
Masahiko Saito ◽  
...  

Author(s):  
Vladislav Izda ◽  
Jake Martin ◽  
Cassandra Sturdy ◽  
Matlock A. Jeffries

Science ◽  
2011 ◽  
Vol 332 (6031) ◽  
pp. 848-852 ◽  
Author(s):  
T. Watanabe ◽  
S.-i. Tomizawa ◽  
K. Mitsuya ◽  
Y. Totoki ◽  
Y. Yamamoto ◽  
...  

2018 ◽  
Author(s):  
Matlock A Jeffries

Autoimmunity refers to a pathologic state of immunologic dysregulation in which the human immune system turns inward, attacking healthy tissues. The key step in this process is a break of self-immune tolerance. Recent studies have implicated dysregulation of gene expression via altered epigenetic control as a key mechanism in the development and promotion of autoimmunity. Epigenetics is defined as heritable changes in gene expression as a result of modification of DNA methylation, histone side chains, and noncoding RNA. Studies examining identical twins discordant for lupus, for example, were among the first to identify alterations in DNA methylation leading to lupus. Histone side-chain changes have been studied extensively in rheumatoid arthritis (RA), and many pathogenic cell types in RA exhibit a hyperacetylation phenotype. Finally, new research in the noncoding RNA field has not only uncovered potentially targetable pathways (e.g., miR-155) but may lead to the development of new diagnostic and prognostic biomarkers, helping physicians better tailor specific treatment regimens to improve response to therapy in autoimmune disease.   This review contains 4 figures, 1 table and 47 references Key Words: autoimmunity, big data, biomarkers, computational biology, DNA methylation, epigenetics, histone acetylation, histone methylation, microRNA, noncoding RNA


2018 ◽  
Vol 115 (48) ◽  
pp. E11321-E11330 ◽  
Author(s):  
Jie Hou ◽  
Xiaowen Shi ◽  
Chen Chen ◽  
Md. Soliman Islam ◽  
Adam F. Johnson ◽  
...  

Changes in dosage of part of the genome (aneuploidy) have long been known to produce much more severe phenotypic consequences than changes in the number of whole genomes (ploidy). To examine the basis of these differences, global gene expression in mature leaf tissue for all five trisomies and in diploids, triploids, and tetraploids of Arabidopsis thaliana was studied. The trisomies displayed a greater spread of expression modulation than the ploidy series. In general, expression of genes on the varied chromosome ranged from compensation to dosage effect, whereas genes from the remainder of the genome ranged from no effect to reduced expression approaching the inverse level of chromosomal imbalance (2/3). Genome-wide DNA methylation was examined in each genotype and found to shift most prominently with trisomy 4 but otherwise exhibited little change, indicating that genetic imbalance is generally mechanistically unrelated to DNA methylation. Independent analysis of gene functional classes demonstrated that ribosomal, proteasomal, and gene body methylated genes were less modulated compared with all classes of genes, whereas transcription factors, signal transduction components, and organelle-targeted protein genes were more tightly inversely affected. Comparing transcription factors and their targets in the trisomies and in expression networks revealed considerable discordance, illustrating that altered regulatory stoichiometry is a major contributor to genetic imbalance. Reanalysis of published data on gene expression in disomic yeast and trisomic mouse cells detected similar stoichiometric effects across broad phylogenetic taxa, and indicated that these effects reflect normal gene regulatory processes.


2018 ◽  
Vol 221 (1) ◽  
pp. 261-278 ◽  
Author(s):  
Francesca Tedeschi ◽  
Paride Rizzo ◽  
Bui Thi Mai Huong ◽  
Andreas Czihal ◽  
Twan Rutten ◽  
...  

2016 ◽  
Vol 62 (4) ◽  
pp. 367-372 ◽  
Author(s):  
Lingling QIU ◽  
Lu XU ◽  
Guobin CHANG ◽  
Qixin GUO ◽  
Xiangping LIU ◽  
...  

Gene ◽  
2019 ◽  
Vol 684 ◽  
pp. 39-46 ◽  
Author(s):  
Jieyun Hong ◽  
Xiaoyu Wang ◽  
Chugang Mei ◽  
Linsen Zan

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