scholarly journals A Long Noncoding RNA, Antisense IL-7, Promotes Inflammatory Gene Transcription through Facilitating Histone Acetylation and Switch/Sucrose Nonfermentable Chromatin Remodeling

2019 ◽  
Vol 203 (6) ◽  
pp. 1548-1559 ◽  
Author(s):  
Xu Liu ◽  
Yajing Lu ◽  
Jie Zhu ◽  
Mingjia Liu ◽  
Minghong Xie ◽  
...  
2016 ◽  
Vol 31 (3) ◽  
pp. 1215-1225 ◽  
Author(s):  
Shibin Ma ◽  
Zhenping Ming ◽  
Ai-Yu Gong ◽  
Yang Wang ◽  
Xiqiang Chen ◽  
...  

2020 ◽  
Vol 14 (5) ◽  
pp. 974-990 ◽  
Author(s):  
Neha Singh ◽  
Sathish K. R. Padi ◽  
Jeremiah J. Bearss ◽  
Ritu Pandey ◽  
Koichi Okumura ◽  
...  

2016 ◽  
Vol 38 (5) ◽  
pp. 375-383 ◽  
Author(s):  
Jessica J. DeWitt ◽  
Patrick M. Hecht ◽  
Nicole Grepo ◽  
Brent Wilkinson ◽  
Oleg V. Evgrafov ◽  
...  

The long noncoding RNA MSNP1AS (moesin pseudogene 1, antisense) is a functional element that was previously associated with autism spectrum disorder (ASD) with genome-wide significance. Expression of MSNP1AS was increased 12-fold in the cerebral cortex of individuals with ASD and 22-fold in individuals with a genome-wide significantly associated ASD genetic marker on chromosome 5p14.1. Overexpression of MSNP1AS in human neuronal cells caused decreased expression of moesin protein, which is involved in neuronal process stability. In this study, we hypothesize that MSNP1AS knockdown impacts global transcriptome levels. We transfected the human neural progenitor cell line SK- N-SH with constructs that caused a 50% suppression of MSNP1AS expression. After 24 h, cells were harvested for total RNA isolation. Strand-specific RNA sequencing analysis indicated altered expression of 1,352 genes, including altered expression of 318 genes following correction for multiple comparisons. Expression of the OAS2 gene was increased >150-fold, a result that was validated by quantitative PCR. Gene ontology analysis of the 318 genes with altered expression following correction for multiple comparisons indicated that upregulated genes were significantly enriched for genes involved in immune response, and downregulated genes were significantly enriched for genes involved in chromatin remodeling. These data indicate multiple transcriptional and translational functions of MSNP1AS that impact ASD-relevant biological processes. Chromatin remodeling and immune response are biological processes implicated by genes with rare mutations associated with ASD. Our data suggest that the functional elements implicated by association of common genetic variants impact the same biological processes, suggesting a possible shared common molecular pathway of ASD.


2018 ◽  
Author(s):  
Jesse R. Raab ◽  
Keriayn N. Smith ◽  
Camarie C. Spear ◽  
Carl J. Manner ◽  
J. Mauro Calabrese ◽  
...  

AbstractSCHLAP1 is a long-noncoding RNA that is prognostic for progression to metastatic prostate cancer and promotes an invasive phenotype. SCHLAP1 is reported to function by depleting the core SWI/SNF subunit, SMARCB1, from the genome. SWI/SNF is a large, multi-subunit, chromatin remodeling complex that can be combinatorially assembled to yield hundreds to thousands of distinct complexes. Here, we investigated the hypothesis that SCHLAP1 affects only specific forms of SWI/SNF and that the remaining SWI/SNF complexes were important for the increased invasion in SCHLAP1 expressing prostate cells. Using several assays we found that SWI/SNF is not depleted from the genome by SCHLAP1 expression. We find that SCHLAP1 induces changes to chromatin openness but is not sufficient to drive changes in histone modifications. Additionally, we show that SWI/SNF binds many coding and non-coding RNAs. Together these results suggest that SCHLAP1 has roles independent of canonical SWI/SNF and that SWI/SNF broadly interacts with RNA.


2016 ◽  
Vol 196 (6) ◽  
pp. 2799-2808 ◽  
Author(s):  
Guoku Hu ◽  
Ai-Yu Gong ◽  
Yang Wang ◽  
Shibin Ma ◽  
Xiqiang Chen ◽  
...  

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Marpadga Reddy ◽  
Zhuo Chen ◽  
Jung‐Tak Park ◽  
Mei Wang ◽  
Linda Lanting ◽  
...  

Blood Science ◽  
2019 ◽  
Vol 1 (2) ◽  
pp. 161-167 ◽  
Author(s):  
Junwei Zhu ◽  
Yunxiao Ren ◽  
Yuanyuan Han ◽  
Tingting Jin ◽  
Yanming Li ◽  
...  

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