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Decoding m6A mRNA methylation by reader proteins in cancer

Cancer Letters, 2021
N6-methyladenosine (m6A), the most prevalent internal modification in eukaryotic mRNAs, regulates gene expression at the post-transcriptional level. The reader proteins of m6A, mainly YTH domain-containing proteins, specifically recognize m6A-modified mRNAs and regulate their metabolism. Recent studies have highlighted essential roles of m6A readers in
Bing Han   +5 more
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Multiple roles of m6A methylation in epithelial–mesenchymal transition

Molecular Biology Reports, 2022
Epithelial-mesenchymal transition (EMT) plays an important role in migration and invasion of cancer cell and the development of tissue fibrosis diseases. N6-methyladenosine (m6A) is the most extensive type of RNA methylation and has aroused extensive interest in recent years.
Xueru Zhao, Xue Li, Xiaohua Li
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m6A mRNA methylation: A pleiotropic regulator of cancer

Gene, 2020
In recent days, RNA modifications are gaining the interest of biologist worldwide. Till date, a total of 171 RNA modifications has been reported, and the number may increase with advancing technologies. The mRNA undergoes modifications like m5M, hm5C, m1A, m6A and pseudouridine, collectively called as epitranscriptomic alterations, each of them has ...
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Role of m6A RNA Methylation in Ischemic Stroke

Molecular Neurobiology
Ischemic stroke is a prominent contributor to global morbidity and mortality rates. The intricate and diverse mechanisms underlying ischemia-reperfusion injury remain poorly comprehended. RNA methylation, an emerging epigenetic modification, plays a crucial role in regulating numerous biological processes, including immunity, DNA damage response ...
Yayun Xu, Wenqiang Liu, Lijie Ren
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m6A RNA methylation regulates mitochondrial function

Human Molecular Genetics
Abstract RNA methylation of N6-methyladenosine (m6A) is emerging as a fundamental regulator of every aspect of RNA biology. RNA methylation directly impacts protein production to achieve quick modulation of dynamic biological processes. However, whether RNA methylation regulates mitochondrial function is not known, especially in neuronal
Michael Kahl   +9 more
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m6A RNA Methylation and Implications for Hepatic Lipid Metabolism

DNA and Cell Biology
This review presents a summary of recent progress in research on the N6-methyladenosine (m6A) modification and regulatory roles in hepatic lipid metabolism. As the most abundant internal modification of eukaryotic RNA, the m6A modification is a dynamic and reversible process of the m6A enzyme system, which includes writers, erasers, and readers.
Xinyue Ming   +5 more
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m6A RNA methylation: The latent string-puller in fibrosis

Life Sciences
Fibrosis is a pathological phenomenon characterized by the aberrant accumulation of extracellular matrix (ECM) in tissues. Fibrosis is a universally age-related disease involving that many organs and is the final stage of many chronic inflammatory diseases, which often threaten the patient's health.
Xinglan, He   +7 more
openaire   +2 more sources

The m6A methylation system limits hepatitis B virus replication

Biomeditsinskaya Khimiya
N6-methyladenosine (m6A) is a common RNA modification, which plays a critical role in RNA fate and regulating such aspects as splicing, stability, nuclear export, and translation efficiency. The introduction, removal, and recognition of m6A modifications in RNA are regulated by a number of factors, known as writer, eraser, and reader proteins.
A V, Kachanov   +6 more
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RNA m6A methylation in psychiatric disorders.

EC psychology and psychiatry
This comprehensive review introduces the features of m6A modification and its role in neuropsychiatric disorders. The research findings suggest that m6A modifications and their regulators play a critical role in the occurrence and development of major psychiatric disorders, especially Alzheimer's disease, affecting synaptic protein synthesis, subtype ...
Qiao, Mao   +7 more
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m6A mRNA methylation drives cardiomyocyte hypertrophy

Journal of Molecular and Cellular Cardiology, 2018
Lisa Dorn   +3 more
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