Project description:To study the gene expression profile difference caused by miR-322/-503 overexpression in the myoblast differentiation of DM1 group, we performed RNA-seq on the total RNA samples collected from the in vitro myoblast differentiation day 4 of control and miR-322/-503 overexpressing DM1 C2C12 cell models. The DM1 cell model was bulit by stably transfecting C2C12 cells with GFP-CUG200 plasmid. Each group contained three biological replicates. The expression matrix was obtained by Hisat2 followed by Stringtie.
Project description:To investigate the effect of miR-503 in aging associated type 2 diabetes, target genes of miR-503 need to be investigated. The global miR-322-503-351 deletion (KO) mouse was constructed, and RNA-seq was then performed on aged mouse liver and white adipose tissue (WAT).
Project description:To study the gene expression profile difference in the myoblast differentiation of normal and DM1 groups, we performed RNA-seq on the total RNA samples collected from the in vitro myoblast differentiation day 4 of normal and DM1 C2C12 cell models. Normal and DM1 cell models were bulit by stably transfecting C2C12 cells with GFP-CUG5 and GFP-CUG200 plasmids. Each group contained three biological replicates. The expression matrix was obtained by Hisat2 followed by Stringtie.
Project description:TGF-β family ligands are key regulators of dendritic cell (DC) differentiation and activation. Epidermal Langerhans cells (LCs) require TGF-β family signaling for their differentiation and canonical TGF-β1 signaling secures a non-activated LC state. LCs reportedly control skin inflammation and are replenished from peripheral blood monocytes, which also give rise to pro-inflammatory monocyte-derived DCs (moDCs). By studying mechanisms in inflammation, we previously screened LCs vs moDCs for differentially expressed miRNAs. miR-424/503 was the most strongly inversely regulated (moDCs > LCs). We found that miR-424/503 is induced during moDC differentiation and promotes moDC differentiation in human and mouse. Inversely, forced repression of miR-424 during moDC differentiation facilitated TGF-β1-dependent LC differentiation. Mechanistically, miR-424/503 deficiency in monocyte/DC precursors leads to the induction of TGF-β1-response genes critical for LC differentiation. Therefore, the miR-424/503 gene cluster plays a decisive role in anti-inflammatory LC vs pro-inflammatory moDC differentiation from monocytes.
Project description:Gene expression profile following transfection with miR-503, miR-103, or miR-494 mature duplex Examination of mRNA levels in HeLa cells following transfection of miR-503, miR-103, or miR-494 mature duplex, control siRNA against GFP, or mock transfection (lipofectamine 2000 alone)
Project description:To have a global picture of the targets of the miR-15 family, we assessed transcriptome changes, by deep-sequencing, of HeLa cells transfected with 3 members of the miR-15 family (miR-15a, miR-16 or miR-503) or a control miRNA (cel-miR-231). We observed a very extensive overlap between the genes down-regulated by these 3 miRNAs, as expected for miRNAs belonging to the same family. transcriptmic profiles of HeLa cells treated miR-15a, miR-16, miR-503 and control-miR were generated by deep sequencing, using Illumina HiSeq2000.