Project description:KMT2B,a major H3K4 tri-methyltransferase, contributes to the development of various cancers. However, its role in cervical cancer is unclear. We found that KMT2B is upregulated in cervical cancer tissues, which is significantly associated with poor prognosis.To investigate the underlying mechanism of KMT2B in the progression of cervical cancer, we established stable KMT2B-overexpression HeLa cells.Then we compared the whole genome mRNA expression profile of KMT2B overexpression and control HeLa cells using RNA-seq.
Project description:The mammalian male germline is sustained by a pool of spermatogonial stem cells (SSCs) that can transmit both genetic and epigenetic information to offspring. However, the mechanisms underlying epigenetic transmission remain unclear. The histone methyltransferase Kmt2b is highly expressed in SSCs and required for the SSC-to-progenitor transition. At the stem cell stage, Kmt2b catalyzes H3K4me3 at bivalent H3K27me3-marked promoters as well as at promoters of a new class of genes lacking H3K27me3, which we call monovalent. Monovalent genes are mainly activated in late spermatogenesis while the bivalent genes are mainly not expressed until embryonic development. These data suggest that SSCs are epigenetically primed by Kmt2b in two distinguishable ways for the upregulation of gene expression during the spermatogenic program and through the male germline into the embryo. Because Kmt2b is also the major H3K4 methyltransferase for bivalent promoters in embryonic stem cells, we also propose that Kmt2b has the capacity to epigenetically prime stem cells.
Project description:MCF-7 is an estrogen receptor-positive breast cancer cell line. This experiment is designed to study (1) the effect of estradiol (E2) exposure and (2) lysine methyltransferase 2B (KMT2B) knockdown in MCF-7 cells. Cells were grown for 72 hours prior to treatment with vehicle or 10 nM E2 for 4 and 24 hours. Additionally, to assess the effect of KMT2B knockdown, MCF-7 cells were transfected with KMT2B targeting siRNA or scrambled control siRNA in the absence or presence of E2. RNA were isolated using Trizol and hybridized to Affymetrix GeneChip Human Genome U133 Plus 2.0 array.
Project description:Transcriptional profiling of all KMT2B-WT, HT, KO, Int iPSCs. KMT2B-HT, KO, and Int iPSCs were generated by gene editing using CRISPR/Cas9 and Cre recombinase technologies.
Project description:This dataset investigates the transcriptional effect of mitochondrial 12S rRNA hypermethylation, both by overexpressing the mitochondrial methyltransferase mtTFB1 in HeLa cells and by using A1555G cybrids, where the 12S rRNA is hypermethylated. HeLa cells overexpressing a methyltransferase-deficient mtTFB1 (mtTFB1[G65A]) and wild-type A1555A cybrids were used as controls.
Project description:HBV-KMT2B integrated human induced pluripotent stem cells (KMT2B-Int iPSCs) vs heterozygous mutated KMT2B iPSCs (KMT2B-HT iPSCs) vs homozygous mutated KMT2B iPSCs (KMT2B-KO iPSCs) vs their original iPSCs (KMT2B-WT iPSCs)
Project description:In order to identify the effects of TFEB overexpression on the hela cells transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the hela TFEB stable clones Transcriptome analysis of hela stable clones overexpressing TFEB-GFP
Project description:In order to identify the effects of TFEB overexpression on the hela cells transcriptome, we performed Affymetrix Gene-Chip hybridization experiments for the hela TFEB stable clones Transcriptome analysis of hela stable clones overexpressing TFEB-3xFLAG
Project description:This dataset investigates the transcriptional effect of mitochondrial 12S rRNA hypermethylation, both by overexpressing the mitochondrial methyltransferase mtTFB1 in HeLa cells and by using A1555G cybrids, where the 12S rRNA is hypermethylated. HeLa cells overexpressing a methyltransferase-deficient mtTFB1 (mtTFB1[G65A]) and wild-type A1555A cybrids were used as controls. four samples with 12S rRNA hypermethylation (two cell lines, with two biological replicates each) versus four samples with basal 12S rRNA methylation (two cell lines, with two biological replicates each)
Project description:Transdifferentiation of fibroblasts into induced Neuronal cells (iNs) by neuronal-specific transcription factors Brn2, Myt1l and Ascl1 is a paradigmatic example of inter-lineage conversion across epigenetically distant cells. Despite tremendous progress on the transcriptional hierarchy underlying transdifferentiation, the enablers of the concomitant epigenome resetting remain to be elucidated. Here we investigated the role of KMT2A and KMT2B, two histone H3 lysine 4 methylases with cardinal roles in development, through individual and combined inactivation. We found that Kmt2b, whose human homologue’s mutations cause dystonia, is selectively required for iN conversion through the suppression of the alternative myocyte program and the induction of neuronal maturation genes.