Project description:The goals of this study are to compare gene expression profiles of Uhrf1 WT and KO germinal center B cells and reveal the underlying mechanisms by which Uhrf1 regulates germinal center B cell responses. We found that upon Uhrf1 depeletion in germinal center B cells, most of the differentially expressed genes were upreguated.
Project description:The goal of this study was to invetigate the mechanisms by which nsd2 regulate germinal center reaction by comparing RNA-seq data between nsd2 wt and ko germinal center B cells
Project description:Deletion of Uhrf1 resulted in stage 1-specific defects during iNKT cell development. To investigate the molecular mechanism, we sorted WT and Uhrf1-KO stage 1 iNKT cells and performed RNA-seq. By comparing gene expression profile, we found metabolic defects in Uhrf1-KO stage 1 iNKT cells. The expression of CD71 (Tfrc), two subunits of CD98 (Slc3a2 and Slc7a5) and Glut3 (Slc2a3) was reduced in stage 1 iNKT cells. Besides, the downstream pathways of AKT-mTOR axis were significantly reduced. Collectively, our results suggest that Uhrf1 is required for iNKT cell development by regulating the Akt-mTOR signaling pathway. We first sorted WT and Uhrf1-KO stage 1 iNKT cells, extracted the mRNA and performed RNA-seq. We then analyzed the differentially expressed genes and performed KEGG pathway analysis. We used RT-PCR to verify the expression of the key nutrient related genes (Tfrc, Slc3a2, Slc7a5 and Slc2a3) and used flow cytometry to test the protein level of metabolic related molecules. Besides, we also analyzed the expression of genes of mTOR downstream pathways to demonstrate that Uhrf1 mediated AKt-mTOR axis regulates iNKT cell development.
Project description:WHSC1 catalyzes dimethylation of lysine 36 on histone H3, which is upregualted in germinal center B cells. This study aimed to understand the H3K36me2 genome-wide alterations by analysing CHIP-seq data between wt and ko germinal center B cells.
Project description:Deletion of Uhrf1 resulted in stage 1-specific defects during iNKT cell development. To investigate the molecular mechanism, we sorted WT and Uhrf1-KO stage 1 iNKT cells and performed RNA-seq. By comparing gene expression profile, we found metabolic defects in Uhrf1-KO stage 1 iNKT cells. The expression of CD71 (Tfrc), two subunits of CD98 (Slc3a2 and Slc7a5) and Glut3 (Slc2a3) was reduced in stage 1 iNKT cells. Besides, the downstream pathways of AKT-mTOR axis were significantly reduced. Collectively, our results suggest that Uhrf1 is required for iNKT cell development by regulating the Akt-mTOR signaling pathway.
Project description:WT-AID-GFP+ and SFR KO-AID-GFP+ mice were immunized with NP(18)OVA+ alum, on Day 9, germinal center B cells (AID-GFP+) were sorted for total RNA
Project description:To understand the mechanisms through which JunB regulates Tregs-mediated immune regulation, we examined the global gene expression profiles in the JunB WT and KO Tregs by performing RNA sequencing (RNA-seq) analysis.
