Project description:control RNA and FTO-IT1 RNA and their interacting proteins were pulled down by biotin-streptavidin beads to see the interacting protein of FTO-IT1 RNA.
Project description:This SuperSeries is composed of the following subset Series: GSE24811: Time Series of Mouse skeletal muscle cell differentiation GSE24852: ChIP-Seq of MyoD, Myf5, Snai1, HDAC1, HDAC2, E47 and empty vector controls in mouse skeletal myoblasts or myotubes GSE38236: RNA-Seq of si-Snai1, si-Snai2, si-Snai1/2 and si-Scrambled treated myoblasts Refer to individual Series
Project description:Increased FTO expression has been connected to resistance to tyrosine kinase inhibitors in CML. To explore the therapeutic potential of targeting FTO in CML, we tested the FTO catalytic inhibitor in the K562 CML cell line. The RNA-seq was performed to identify relevant regulated genes.
Project description:Genome-wide association studies in diverse populations have reproducibly associated variants within introns of FTO with increased risk for obesity and type-2 diabetes.While the molecular mechanisms linking these noncoding variants with obesity are not immediately obvious, subsequent studies in mice demonstrated that FTO expression levels influence body mass and composition phenotypes. Yet, no direct connection between the obesity-associated intronic variants and FTO expression or function has been made. We show that the obesity-associated noncoding sequences within FTO are functionally connected, at megabase distances, primarily with the homeobox gene IRX3, rather than with FTO. 4C-seq samples for Fto/fto and Irx3/irx3a genes promoters in different samples: adult mouse brain, E9.5 mouse embryos and 24hpf zebrafish embryos.
Project description:To determine the potential targets of FTO and identify treatment significance of FTO inhibition in AML, we conducted transcriptome wide RNA seq with NB4 cells upon DMSO and FTO inhibitors (FB23 and FB23-2) treatment.
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:To gain insight into FTO function, we knocked down and overexpressed FTO in HEK293 cells.Genetrail analyses of expression profiles pointed to the RNA splicing and processing machinery. Intriguingly, using immunocytochemistry and confocal laser scanning microscopy, we observed strong enrichment of FTO in nuclear speckles and - to a lesser extent - in nucleoli, but not in other known nuclear bodies. We also studied RNA samples of Fto knockout and wild type mice with regard to content of methylated and unmethylated nucleosidesand observed that ratios of modified and unmodified uracil and adenine were different depending on the presence of FTO. Taken together, our data suggest that FTO is involved in RNA processing and modification. We used microarrays to investigate global gene expression changes depending on the level of FTO We compared FTO overexpressing and FTO depleted cells to cells with endogeneus level of FTO to determine global gene expression changes.
Project description:To identify the expression of mRNAs after knockdown of FTO, we performed RNA-Seq in MA9.3ITD cells with or without knockdown of FTO.