Results 11 to 20 of about 23,713 (215)

N6-Methyladenosine-Sculpted Regulatory Landscape of Noncoding RNA

open access: yesFrontiers in Oncology, 2021
The exploration of dynamic N6-methyladenosine (m6A) RNA modification in mammalian cells has attracted great interest in recent years. M6A modification plays pivotal roles in multiple biological and pathological processes, including cellular reprogramming,
Zhongyuan Zhang   +3 more
doaj   +1 more source

The Potential Role of m6A RNA Methylation in the Aging Process and Aging-Associated Diseases

open access: yesFrontiers in Genetics, 2022
N6-methyladenosine (m6A) is the most common and conserved internal eukaryotic mRNA modification. m6A modification is a dynamic and reversible post-transcriptional regulatory modification, initiated by methylase and removed by RNA demethylase. m6A-binding
Jin Sun   +19 more
doaj   +1 more source

The role of regulators of RNA m6A methylation in lung cancer

open access: yesGenes and Diseases, 2023
N6-methyladenosine (m6A) modification is found the most prevalent and abundant post-transcriptional mRNA modification in eukaryotic cells. It regulates almost all stages of RNA life cycle including splicing, translocation, stability, decay and ...
Qicheng Zhang, Ke Xu
doaj   +1 more source

The crucial roles of N6-methyladenosine (m6A) modification in the carcinogenesis and progression of colorectal cancer

open access: yesCell & Bioscience, 2021
As the predominant modification in RNA, N6-methyladenosine (m6A) has attracted increasing attention in the past few years since it plays vital roles in many biological processes.
Zhihao Fang   +5 more
doaj   +1 more source

Analysis of m6A Methylation Modification Patterns and Tumor Immune Microenvironment in Breast Cancer

open access: yesFrontiers in Cell and Developmental Biology, 2022
Increasing evidence indicates that the abnormal expression of N6-methyladenosine (m6A) modification is closely related to the epigenetic regulation of immune response in breast cancer (BC).
Menglu Dong   +4 more
doaj   +1 more source

The functions of N6-methyladenosine modification in lncRNAs

open access: yesGenes and Diseases, 2020
Increasing evidence indicates that mRNAs are often subject to posttranscriptional modifications. Among them, N6-methyladenosine (m6A), which has been shown to play key roles in RNA splicing, stability, nuclear export, and translation, is the most ...
Rong-Zhang He, Jing Jiang, Di-Xian Luo
doaj   +1 more source

N6-Methyladenosine modification: a novel pharmacological target for anti-cancer drug development

open access: yesActa Pharmaceutica Sinica B, 2018
N6-Methyladenosine (m6A) modification is the most pervasive modification of human mRNA molecules. It is reversible via regulation of m6A modification methyltransferase, demethylase and proteins that preferentially recognize m6A modification as “writers”,
Yi Niu   +4 more
doaj   +1 more source

m6A Methylation in Cardiovascular Diseases: From Mechanisms to Therapeutic Potential

open access: yesFrontiers in Genetics, 2022
Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide. Recent studies have shown that n6-methyladenosine (m6A) plays a major role in cardiovascular homeostasis and pathophysiology.
Longbo Li   +5 more
doaj   +1 more source

Characterization of the m6A regulator-mediated methylation modification patterns in oral squamous cell carcinoma

open access: yesScientific Reports, 2023
N 6-methyladenosine (m6A) is a form of posttranscriptional modification that plays important roles in cancer including oral squamous cell carcinoma (OSCC).
Lu Pan   +6 more
doaj   +1 more source

The Potential Roles of RNA N6-Methyladenosine in Urological Tumors

open access: yesFrontiers in Cell and Developmental Biology, 2020
N6-methyladenosine (m6A) is regarded as the most abundant, prevalent and conserved internal mRNA modification in mammalian cells. M6A can be catalyzed by m6A methyltransferases METTL3, METTL14 and WTAP (writers), reverted by demethylases ALKBH5 and FTO ...
Yang Li   +5 more
doaj   +1 more source

Home - About - Disclaimer - Privacy