Project description:To investigate the gene expression signatures of ICAM-1 candidate negative regulator UHRF1, we generate the UHRF1 KO cells and profiled the transcriptome changes by paired-end RNA seq.
Project description:To investigate the funciton of UHRF1 in ICAM1 and pro-inflammatory genes regulaiton, we generate the UHRF1 KO cells and profiled the WGBS.
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: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: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:RNAseq was used to identify host and viral transcriptome changes in UHRF1 knock-out RaeL cells. UHRF1 KO RaeL cells were subjected to FACSort for ICAM1+ subpopulations, which were further used for RNAseq analysis. The RaeL cells expressing control sgRNA was used as the control.
Project description:We used miRNA microarrays to detail the miRNA content in A549 Ago2-KO/HA-Ago2Wt, Ago2-KO/HA-Ago2KA, and Ago2-KO/HA-Ago2Δ (Dm) cells
Project description:RNAseq was used to identify host and viral transcriptome changes in UHRF1 knock-out MUTU I cells. UHRF1 KO MUTU I cells were subjected to FACSort for ICAM1+/GP350- and ICAM1-/GP350+ subpopulations, which were further used for RNAseq analysis. The MUTU I cells expressing control sgRNA was used as the control.