Project description:Here we use MeRIP-Seq to analyze global adenosine methylation (m6A) in mRNAs in the midbrain and striatum of Fto-deficient mice. We find that Fto deficiency leads to increased methylation within a subset of mRNAs important for neuronal signaling, including many within the dopaminergic signaling pathway. Collectively, our results show that Fto regulates demethylation of specific mRNAs in vivo, and this activity relates to control of dopaminergic transmission. Profiling of m6A in midbrain and striatum from FTO knockout mice
Project description:Here we use MeRIP-Seq to analyze global adenosine methylation (m6A) in mRNAs in the midbrain and striatum of Fto-deficient mice. We find that Fto deficiency leads to increased methylation within a subset of mRNAs important for neuronal signaling, including many within the dopaminergic signaling pathway. Collectively, our results show that Fto regulates demethylation of specific mRNAs in vivo, and this activity relates to control of dopaminergic transmission. Profiling of m6A in midbrain and striatum from wild type mice
Project description:Cardiac fibrosis is common in cardiovascular diseases. N6-methyladenosine (m6A) is one of the most common modifications in eukaryotic mRNAs. Previous research has suggested that m6A modification is vital in cardiovascular diseases. The underlying targets of FTO were selected through transcriptome sequencing (RNA-seq) combined with methylated RNA immunoprecipitation sequencing (MeRIP-seq). According to MeRIP-seq and RNA-seq, FTO inhibited collagen synthesis in CFs.
Project description:Cardiac fibrosis is common in cardiovascular diseases. N6-methyladenosine (m6A) is one of the most common modifications in eukaryotic mRNAs. Previous research has suggested that m6A modification is vital in cardiovascular diseases. The underlying targets of FTO were selected through transcriptome sequencing (RNA-seq) combined with methylated RNA immunoprecipitation sequencing (MeRIP-seq). According to MeRIP-seq and RNA-seq, FTO inhibited collagen synthesis in CFs.
Project description:We tried to analyze the effect of FTO on papillary thyroid carcinoma. We constructed a FTO overexpression stable cell line of papillary thyroid carcinoma cells. We performed meRIP-seq sequencing analysis of the FTO overexpression stable transfer cell line to try to assess which genes were changed at the m6A level in papillary thyroid cancer cells by overexpressing FTO.
Project description:We tried to analyze the effect of FTO on papillary thyroid carcinoma. We constructed a FTO overexpression stable cell line of papillary thyroid carcinoma cells. We performed meRIP-seq sequencing analysis of the FTO overexpression stable transfer cell line to try to assess which genes were changed at the m6A level in papillary thyroid cancer cells by overexpressing FTO.
Project description:Only a few studies have attempted to explore the potential role of FTO in gastric cancer, with one focusing on mitochondrial metabolism, while others have focused on the association of FTO with cell proliferation, migration, and invasion. To date, no study has comprehensively linked FTO-dependent m6A methylation to any form of cell death. We comprehensively explore the role of FTO-mediated m6A modification in gastric cancer ferroptosis by MeRIP-seq.
Project description:Here we use MeRIP-Seq to analyze global adenosine methylation (m6A) in mRNAs in the midbrain and striatum of Fto-deficient mice. We find that Fto deficiency leads to increased methylation within a subset of mRNAs important for neuronal signaling, including many within the dopaminergic signaling pathway. Collectively, our results show that Fto regulates demethylation of specific mRNAs in vivo, and this activity relates to control of dopaminergic transmission.
Project description:Here we use MeRIP-Seq to analyze global adenosine methylation (m6A) in mRNAs in the midbrain and striatum of Fto-deficient mice. We find that Fto deficiency leads to increased methylation within a subset of mRNAs important for neuronal signaling, including many within the dopaminergic signaling pathway. Collectively, our results show that Fto regulates demethylation of specific mRNAs in vivo, and this activity relates to control of dopaminergic transmission.
Project description:To investigate the mechanism of demethylase FTO in Crohn's disease，We used m6A MeRIP-seq data from three normal colon samples and three TNBS-induced IBD colon samples of C57 mice for gene expression profiling.
