Long non-coding RNA regulation of gene expression during differentiation

2016 ◽  
Vol 468 (6) ◽  
pp. 971-981 ◽  
Author(s):  
Vanessa Lopez-Pajares
Keyword(s):  
Gene Expression ◽  
Regulation Of Gene Expression ◽  
Rna Regulation ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Regulatory Non-coding RNAs for Death Associated Protein Kinase Family

2021 ◽  
Vol 8 ◽  
Author(s):  
Qingshui Wang ◽  
Youyu Lin ◽  
Wenting Zhong ◽  
Yu Jiang ◽  
Yao Lin
Keyword(s):  
Gene Expression ◽  
Current Knowledge ◽  
Regulation Of Gene Expression ◽  
Tumor Development ◽  
Invasion And Metastasis ◽  
Calcium Dependent ◽  
Non Coding Rna ◽  
Death Associated Protein Kinase ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

The death associated protein kinases (DAPKs) are a family of calcium dependent serine/threonine kinases initially identified in the regulation of apoptosis. Previous studies showed that DAPK family members, including DAPK1, DAPK2 and DAPK3 play a crucial regulatory role in malignant tumor development, in terms of cell apoptosis, proliferation, invasion and metastasis. Accumulating evidence has demonstrated that non-coding RNAs, including microRNA (miRNA), long non-coding RNA (lncRNA) and circRNA, are involved in the regulation of gene expression and tumorigenesis. Recent studies indicated that non-coding RNAs participate in the regulation of DAPKs. In this review, we summarized the current knowledge of non-coding RNAs, as well as the potential miRNAs, lncRNAs and circRNAs, that are involved in the regulation of DAPKs.

scholarly journals Sox2-RNA mechanisms of chromosome topological control in developing forebrain

2020 ◽  
Author(s):  
Ivelisse Cajigas ◽  
Abhijit Chakraborty ◽  
Madison Lynam ◽  
Kelsey R Swyter ◽  
Monique Bastidas ◽  
...  
Keyword(s):  
Gene Expression ◽  
Long Range ◽  
Target Genes ◽  
Regulation Of Gene Expression ◽  
Interaction Sites ◽  
Non Coding Rna ◽  
Selective Targeting ◽  
Chromosome Topology ◽  
Key Sites ◽  
Long Non Coding Rna

SummaryPrecise regulation of gene expression networks requires the selective targeting of DNA enhancers. The Evf2 long non-coding RNA regulates Dlx5/6 ultraconserved enhancer(UCE) interactions with long-range target genes, controlling gene expression over a 27Mb region in mouse developing forebrain. Here, we show that Evf2 long range gene repression occurs through multi-step mechanisms involving the transcription factor Sox2, a component of the Evf2 ribonucleoprotein complex (RNP). Evf2 directly interacts with Sox2, antagonizing Sox2-dependent Dlx5/6UCE activation. Evf2 regulates Sox2 binding at key sites, including the Dlx5/6eii shadow enhancer and Dlx5/6UCE interaction sites. Evf2 differentially targets RNP-associated Sox2 protein pools (PPs), redirecting Sox2-PPs to one repressed gene at the expense of the other. Co-regulation of Dlx5/6UCEintrachromosomal interactions by Evf2 and Sox2 reveals a role for Sox2 in chromosome topology. We propose that RNA organizes RNPs in a subnuclear domain, regulating both long-range UCE targeting and activity through Sox2-RNP sequestration and recruitment.

Antisense Long Non-Coding RNA in the Regulation of Gene Expression

2013 ◽  
Vol 29 (7) ◽  
pp. 471
Author(s):  
Xiaoming JIANG ◽  
Yongfu SHAO ◽  
Bingxiu XIAO ◽  
Junming GUO
Keyword(s):  
Gene Expression ◽  
Regulation Of Gene Expression ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Functional impacts of non-coding RNA processing on enhancer activity and target gene expression

2019 ◽  
Vol 11 (10) ◽  
pp. 868-879 ◽  
Author(s):  
Evgenia Ntini ◽  
Annalisa Marsico
Keyword(s):  
Gene Expression ◽  
Rna Processing ◽  
Regulation Of Gene Expression ◽  
Regulatory Elements ◽  
Transcription Unit ◽  
Supporting Evidence ◽  
Enhancer Activity ◽  
Rna Transcripts ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Tight regulation of gene expression is orchestrated by enhancers. Through recent research advancements, it is becoming clear that enhancers are not solely distal regulatory elements harboring transcription factor binding sites and decorated with specific histone marks, but they rather display signatures of active transcription, showing distinct degrees of transcription unit organization. Thereby, a substantial fraction of enhancers give rise to different species of non-coding RNA transcripts with an unprecedented range of potential functions. In this review, we bring together data from recent studies indicating that non-coding RNA transcription from active enhancers, as well as enhancer-produced long non-coding RNA transcripts, may modulate or define the functional regulatory potential of the cognate enhancer. In addition, we summarize supporting evidence that RNA processing of the enhancer-associated long non-coding RNA transcripts may constitute an additional layer of regulation of enhancer activity, which contributes to the control and final outcome of enhancer-targeted gene expression.

scholarly journals Epigenetic Insights and Potential Modifiers as Therapeutic Targets in β–Thalassemia

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 755
Author(s):  
Nur Atikah Zakaria ◽  
Md Asiful Islam ◽  
Wan Zaidah Abdullah ◽  
Rosnah Bahar ◽  
Abdul Aziz Mohamed Yusoff ◽  
...  
Keyword(s):  
Gene Expression ◽  
Clinical Presentation ◽  
Globin Gene ◽  
Fetal Hemoglobin ◽  
Dna Hypomethylation ◽  
Considerable Research ◽  
Non Coding Rna ◽  
Hbf Level ◽  
Long Non Coding Rna ◽  
Globin Gene Expression

Thalassemia, an inherited quantitative globin disorder, consists of two types, α– and β–thalassemia. β–thalassemia is a heterogeneous disease that can be asymptomatic, mild, or even severe. Considerable research has focused on investigating its underlying etiology. These studies found that DNA hypomethylation in the β–globin gene cluster is significantly related to fetal hemoglobin (HbF) elevation. Histone modification reactivates γ-globin gene expression in adults and increases β–globin expression. Down-regulation of γ–globin suppressor genes, i.e., BCL11A, KLF1, HBG-XMN1, HBS1L-MYB, and SOX6, elevates the HbF level. β–thalassemia severity is predictable through FLT1, ARG2, NOS2A, and MAP3K5 gene expression. NOS2A and MAP3K5 may predict the β–thalassemia patient’s response to hydroxyurea, a HbF-inducing drug. The transcription factors NRF2 and BACH1 work with antioxidant enzymes, i.e., PRDX1, PRDX2, TRX1, and SOD1, to protect erythrocytes from oxidative damage, thus increasing their lifespan. A single β–thalassemia-causing mutation can result in different phenotypes, and these are predictable by IGSF4 and LARP2 methylation as well as long non-coding RNA expression levels. Finally, the coinheritance of β–thalassemia with α–thalassemia ameliorates the β–thalassemia clinical presentation. In conclusion, the management of β–thalassemia is currently limited to genetic and epigenetic approaches, and numerous factors should be further explored in the future.

Biochemical study on long non coding RNA gene expression in women having preeclampsia

Gene Reports ◽  
2021 ◽  
pp. 101257
Author(s):  
Eman Masoud Abd El Gayed ◽  
Ibrahim Fathi Zaid ◽  
Alaa Masoud Abd El Gayed ◽  
Aziza Mahmoud Mohamed Zaki ◽  
Eman Abd-allah Mahmoud Fouda
Keyword(s):  
Gene Expression ◽  
Biochemical Study ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract TMP25: Long Non-Coding RNA Mediates Stroke-Induced Neurogenesis

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Baoyan Fan ◽  
Wanlong Pan ◽  
Xinli Wang ◽  
Michael Chopp ◽  
Zheng Gang Zhang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Regulation Of Gene Expression ◽  
Artery Occlusion ◽  
Loss Of Function ◽  
Bioinformatics Analyses ◽  
Guide Rna ◽  
Non Coding Rna ◽  
Cerebral Artery Occlusion ◽  
Long Non Coding Rna

Background and Purpose: Adult neurogenesis contributes to functional recovery after stroke. Long non-coding RNAs (lncRNAs) regulate stem cell self-renewal and differentiation. However, the role of lncRNAs in stroke-induced neurogenesis remains unknown. Methods and Results: Using lncRNA array and in situ hybridization, we analyzed lncRNA profiles of adult neural stem cells (NSCs) isolated from the subventricular zone neurogenic region in rats subjected to middle cerebral artery occlusion. We found that H19 was the most highly upregulated lncRNA (19 fold) in ischemic NSCs compared with non-ischemic NSCs. Reduction of endogenous H19 in NSCs by CRISPR-Cas9 genome editing significantly decreased the proliferation and increased the apoptosis of ischemic NSCs, as assayed by the number of BrdU + cells (56±5% vs 22±3%, p<0.01, n=3) and Caspase-3/7 activity compared to NSCs transfected with scrambled small guide RNA (sgRNA). Knockdown of H19 significantly decreased the number of Tuj1 + neuroblasts (8±2% vs 5±0.4%, p<0.01, n=3) and NG 2 + oliogodendrocyte progenitor cells (10±1% vs 5±0.3%, p<0.01, n=3), suggesting that deletion of H19 suppresses the proliferation and survival and blocks the differentiation of NSCs into neurons and oligodendrocytes. Additional RNA-sequencing and bioinformatics analyses revealed that genes deregulated by H19 knockdown were involved in transcription, apoptosis, proliferation, cell cycle and response to hypoxia. Western blot analysis validated that loss-of-function and gain-of-function of H19 significantly increased and reduced, respectively, the transcription of cell cycle-related genes including p27. Using ChIRP assay, we found that upregulated H19 in NSCs was physically associated with EZH2 which catalyzes the repressive H3K27me3 histone marker. Knockdown of H19 significantly reduced the enrichment of H3K27me3 at the promoter of p27, leading to the upregulation of p27 expression and consequently inhibition of NSC proliferation. Conclusions: H19 mediates stroke-induced neurogenesis by regulating genes involved in cell cycle and survival through the interaction with chromatin remodeling proteins. Our data provide novel insights into epigenetic regulation of gene expression by lncRNA in neurogenesis.

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