Faculty Opinions recommendation of Epigenetic regulator UHRF1 inactivates REST and growth suppressor gene expression via DNA methylation to promote axon regeneration.

2019 ◽  
Author(s):  
Phillip G Popovich
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Axon Regeneration ◽  
Suppressor Gene ◽  
Epigenetic Regulator ◽  
Growth Suppressor

scholarly journals Epigenetic regulator UHRF1 inactivates REST and growth suppressor gene expression via DNA methylation to promote axon regeneration

2018 ◽  
Vol 115 (52) ◽  
pp. E12417-E12426 ◽  
Author(s):  
Young Mi Oh ◽  
Marcus Mahar ◽  
Eric E. Ewan ◽  
Kathleen M. Leahy ◽  
Guoyan Zhao ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Tumor Suppressor ◽  
Axon Regeneration ◽  
Ring Finger ◽  
Suppressor Gene ◽  
Dna Methyltransferases ◽  
Epigenetic Mechanism ◽  
Nerve Lesion ◽  
Axon Injury ◽  
Epigenetic Regulator

Injured peripheral sensory neurons switch to a regenerative state after axon injury, which requires transcriptional and epigenetic changes. However, the roles and mechanisms of gene inactivation after injury are poorly understood. Here, we show that DNA methylation, which generally leads to gene silencing, is required for robust axon regeneration after peripheral nerve lesion. Ubiquitin-like containing PHD ring finger 1 (UHRF1), a critical epigenetic regulator involved in DNA methylation, increases upon axon injury and is required for robust axon regeneration. The increased level of UHRF1 results from a decrease in miR-9. The level of another target of miR-9, the transcriptional regulator RE1 silencing transcription factor (REST), transiently increases after injury and is required for axon regeneration. Mechanistically, UHRF1 interacts with DNA methyltransferases (DNMTs) and H3K9me3 at the promoter region to repress the expression of the tumor suppressor gene phosphatase and tensin homolog (PTEN) and REST. Our study reveals an epigenetic mechanism that silences tumor suppressor genes and restricts REST expression in time after injury to promote axon regeneration.

Nitric oxide is an epigenetic regulator of gene expression by directly controlling DNA methylation patterns

2018 ◽  
Vol 120 ◽  
pp. S114 ◽  
Author(s):  
Rhea Bovee ◽  
Vy Pham ◽  
Jenna Fernandez ◽  
Natalia Tretyakova ◽  
Douglas D. Thomas
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Dna Methylation ◽  
Epigenetic Regulator ◽  
Methylation Patterns

scholarly journals Critical Role of Histone Methylation in Tumor Suppressor Gene Silencing in Colorectal Cancer

2003 ◽  
Vol 23 (1) ◽  
pp. 206-215 ◽  
Author(s):  
Yutaka Kondo ◽  
LanLan Shen ◽  
Jean-Pierre J. Issa
Keyword(s):  
Gene Expression ◽  
Colorectal Cancer ◽  
Dna Methylation ◽  
Gene Silencing ◽  
Dna Methyltransferase ◽  
Critical Role ◽  
Histone H3 ◽  
Suppressor Gene ◽  
Promoter Dna Methylation ◽  
Promoter Dna

ABSTRACT The mechanism of DNA hypermethylation-associated tumor suppressor gene silencing in cancer remains incompletely understood. Here, we show by chromatin immunoprecipitation that for three genes (P16, MLH1, and the O 6-methylguanine-DNA methyltransferase gene, MGMT), histone H3 Lys-9 methylation directly correlates and histone H3 Lys-9 acetylation inversely correlates with DNA methylation in three neoplastic cell lines. Treatment with the histone deacetylase inhibitor trichostatin A (TSA) resulted in moderately increased Lys-9 acetylation at silenced loci with no effect on Lys-9 methylation and minimal effects on gene expression. By contrast, treatment with the DNA methyltransferase inhibitor 5-aza-2′-deoxycytidine (5Aza-dC) rapidly reduced Lys-9 methylation at silenced loci and resulted in reactivation for all three genes. Combined treatment with 5Aza-dC and TSA was synergistic in reactivating gene expression through simultaneous effects on Lys-9 methylation and acetylation, which resulted in a robust increase in the ratio of Lys-9 acetylated and methylated histones at loci showing dense DNA methylation. By contrast to Lys-9, histone H3 Lys-4 methylation inversely correlated with promoter DNA methylation, was not affected by TSA, and was increased moderately at silenced loci by 5Aza-dC. Our results suggest that reduced H3 Lys-4 methylation and increased H3 Lys-9 methylation play a critical role in the maintenance of promoter DNA methylation-associated gene silencing in colorectal cancer.

scholarly journals A 5′- Regulatory Region and Two Coding Region Polymorphisms Modulate Promoter Activity and Gene Expression of the Growth Suppressor Gene ZBED6 in Cattle

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e79744 ◽  
Author(s):  
Yong-Zhen Huang ◽  
Ming-Xun Li ◽  
Jing Wang ◽  
Zhao-Yang Zhan ◽  
Yu-Jia Sun ◽  
...  
Keyword(s):  
Gene Expression ◽  
Promoter Activity ◽  
Regulatory Region ◽  
Suppressor Gene ◽  
Coding Region ◽  
Growth Suppressor

scholarly journals Epigenetic Studies of Atopic Dermatitis

2020 ◽  
Author(s):  
Vladimir Sobolev ◽  
Elizaveta Bystritskaya ◽  
Oxana Svitich
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Atopic Dermatitis ◽  
Nucleotide Sequence ◽  
T Lymphocyte ◽  
Population Genetic ◽  
Regulatory Mechanisms ◽  
Adaptive Immune ◽  
Epigenetic Regulator ◽  
Activity Of Enzymes

Since the pathogenesis of atopic dermatitis could not be explained only by a population genetic and phenotypic profiles, epigenetic regulator factors have been considered. Epigenetics is the study of inherited changes in gene expression that are not related to changes in its nucleotide sequence. One of the main classical regulatory mechanisms in human cells is DNA methylation. It is not clear how permanent modifications caused by this process are and whether it is possible to affect them by changing the activity of enzymes that trigger remodeling reactions. In this chapter we analyze all recent studies in this field. We focus more on methylation of innate and adaptive immune factors, with an emphasis on T-lymphocyte genes such as CD3, CD4, and CD8.

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