Project description:KMT2D is a histone methyltransferase for catalyzing the monomethylation of H3K4. Previous studies have indentified that H3K4me1 is prominent on active enhancers and participates in gene expression regulation. To further examine the transcriptional changes in response to KMT2D depletion, we performed RNA-seq with KMT2D knockdown and control PC-3 cells by BGISEQ-500
Project description:KMT2D is a histone methyltransferase for catalyzing the monomethylation of H3K4. The H3K4me1 is prominent on active enhancers and participates in gene expression regulation. Loss of KMT2D in cancer has been approved to impact on a set of gene expression by the reduction of H3K4me1 level. To identify the direct target of KMT2D in prostate cancer, we performed H3K4me1 ChIP-seq with KMT2D knockdown and control PC-3 cells.
Project description:Purpose: Study of the mechanism trough which KTM2D regulates chromatin modification and transcription in a xenograft model of human metatstatic melanoma Methods: We generated patient derived xenografts (PDXs) from metastatic melanoma (MM) biopsies of three different patients. The MMs carry NRASQ61L, NRASQ61Q or BRAFV600 mutations. Cells from secondary PDX (PDX2) were transduced with lentiviral vectors carrying Luciferase (shLuc) and KMT2D (shKMT2D) hairpins and mRNA profiles and genome-wide chromatin-state maps were generated by deep sequencing using Illumina HiSeq2000. Results: we found that KMT2D regulates the activity of a subset of enhancers required for expression of specific genes.
Project description:We report the high-throughput profiling of histone modifications( H3K4me3 and H3K27ac) inTRIM11 knockdown and KDM5C knockdown MDA-MB-231 cells. we generated genome-wide chromatin-state maps of MDA-MB-231 cells.This study provides the localization of H3K4me3 and H3K27ac on chromatin in TRIM11 knockdown and KDM5C knockdown MDA-MB-231 cells.