Project description:N6-methyladenosine (m6A) is one of the most popular RNA modifications, which is widely found in messenger RNAs (mRNAs) and non-coding RNA like long no-coding RNA (lncRNAs) and circular RNA (circRNAs).In our study,we provide m6A landscape of human ameloblastoma, which expands the understanding of m6A modifications and uncovers regulation of lncRNAs and circRNAs through m6A modification in ameloblastoma.
Project description:To identify the N6-methyladenosine (m6A) modified circular RNAs (circRNAs) involved in a mouse model of oxygen-induced retinopathy (OIR), microarray analysis was performed with the retinal samples from OIR mice and Room air controls.
Project description:Morphine tolerance is a tricky problem, the mechanism of it is still unclear. Circular RNAs (CircRNAs) play important roles in biological process of central nervous system. N6-methyladenosine (m6A) as a key post-transcriptional modification of RNA can regulate the metabolism and functions of circRNAs. Here we conducted this research to explore the patterns of m6A-methylation of circRNAs in the spinal cords of 4 morphine tolerated rats and 4 normal rats.
Project description:To explore the involvement of N6-methyladenosine (m6A) modification in circular RNAs (circRNAs) and relevant methyltransferases in the lesion of lens epithelium cells (LECs) under the circumstances of age-related cataract (ARC).
Project description:N6-methyladenosine (m6A) is the most abundant internal messenger (mRNA) modification in mammalian mRNA. This modification is reversible and non-stoichiometric, which potentially adds an additional layer of variety and dynamic control of mRNA metabolism. The m6A-modified mRNA can be selectively recognized by the YTH family “reader” proteins. The preferential binding of m6A-containing mRNA by YTHDF2 is known to reduce the stability of the target transcripts; however, the exact effects of m6A on translation has yet to be elucidated. Here we show that another m6A reader protein, YTHDF1, promotes ribosome loading of its target transcripts. YTHDF1 forms a complex with translation initiation factors to elevate the translation efficiency of its bound mRNA. In a unified mechanism of translation control through m6A, the YTHDF2-mediated decay controls the lifetime of target transcripts; whereas, the YTHDF1-based translation promotion increases the translation efficiency to ensure effective protein production from relatively short-lived transcripts that are marked by m6A. PAR-CLIP and RIP was used to identify YTHDF1 binding sites followed by ribosome profling and RNA seq to assess the consequences of YTHDF1 siRNA knock-down