Project description:Previous works showed that gata4/5/6 lie at the hierarchical apex of the regulatory network of the hemangioblast formation and primitive myelopoiesis in zebrafish. To explore the roles of miRNAs in zebrafish primitive myelopoiesis, we employed deep sequencing to analyze the difference of miRNA expression profiles between gata4/5/6 knockdown embryos (gata5/6 morphants) and control embryos.
Project description:Zebrafish gata4/5/6 are known to lie on the apex of the regulatory hierarchy in primitive myelopoiesis. However, little is known about the roles of microRNAs in this process. Performing microarray analysis on the expression changes of microRNAs in the gata4/5/6 knockdown embryos, we found that miR-210-5p is a novel regulator in zebrafish primitive myelopoiesis. To uncover the target genes of miR-210-5p to mediate its role in inhibiting zebrafish primitive myelopoiesis, we performed microarray analysis to identify differentially expressed genes in gata4/5/6 knockdown embryos.
Project description:The expression level of mRNA after knocking-down lncRNA-MEG3 showed a great significance. We performed microarray and transcriptome profiling in C2C12 cells after transfection lncRNA-MEG3 48 hours later to detail the expression of mRNA after knocking-down lncRNA-MEG3.
Project description:Three transcription factors KLF5, GATA4 and GATA6 are recurrently amplified in multiple gastric cancer cohorts, representing one type of lineage-survival oncogenes in gastric cancer. ChIP-Seq analysis of these three factors in multiple cell lines revealed that significant number of genomic sites are co-occupied by KLF5 and GATA4 and/or GATA6. Integrative analysis of ChIP-Seq and gene expression identified several targets of the three transcription factors in both cell lines and primary tumors, including HNF4A. These results suggest that KLF5, GATA4 and GATA6 interact and co-operate to regulate HNF4A and other genes to promote tumorigenesis in gastric cancer. Gene expression profiling of KLF5, GATA4 and GATA6 knock down in YCC3/AGS/KATOIII cells