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Mouse single positive thymocyte bulk RNA-seq from Kmt2d knockout and control littermates.

ABSTRACT: Mouse single positive thymocyte bulk RNA-seq from Kmt2d knockout and control littermates.

PROVIDER: PRJNA844331 | ENA |

REPOSITORIES: ENA

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Mouse single positive thymocyte bulk RNA-seq from Kmt2d knockout and control littermates.

Project description:To evaluate the hypothesis that dysregulated thymocyte development contributes to immune deficiencies in individuals with KS1. We generated bulk murine CD4+ or CD8+ single positive thymocyte RNA-seq data from cells which lack the histone methyltransferase, Kmt2d SET domain (exons 50/51), with a conditional Cre-recombinase driven by Lck-CreMar (T cell specific) or Vav1-iCre (hematopoietic). Expression profiling by high throughput sequencing.

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RNA-seq of KMT2D Knockout and KMT2D WT melanoma in mice

Project description:Somatic mutations in various epigenetic regulators, including histone methyltransferases KMT2C and KMT2D, have emerged as important cancer-driving events. However, the mechanism of action and therapeutic vulnerability imparted by these mutations remain poorly understood. We identified KMT2D and 8 other epigenetic regulators as potential suppressors to melanoma initiation through an in vivo pooled epigenome-focused RNAi screen. Loss of KMT2D, which exhibits somatic mutations in human melanoma and other cancers, drastically enhanced melanoma progression in xenograft models and a BRAFV600E-driven genetically engineered mouse model of melanoma. Epigenome profiling of 6 histone marks and chromatin state alterations showed substantial reprogramming of H3K4me1- and H3K27ac-marked active enhancer states in KMT2D mutant tumors. Energy metabolic pathways such as glycolysis, OxPhos and TCA/electron transport showed high degree of deregulation which was confirmed with metabolic profiling. Pharmacological abrogation of glycolysis led to reduced proliferation and tumorigenesis preferentially in KMT2D mutant cells. Mechanistically, we find that enhancer loss at IGFBPs increases IGF signaling and downstream AKT phosphorylation that leads to upregulation of metabolic pathways rendering KMT2D mutant cells dependent on these energy metabolism pathways for their higher growth potential. Overall, we present evidence that KMT2D mutations promote tumorigenesis by reprogramming energy metabolism pathways through enhancer reprogramming.

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Genome-wide maps of chromatin state in KMT2D Knockout and KMT2D WT melanoma in mice

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RNA-seq data from double positive thymocyte and CD4 or CD8 single positive spleen T cell

Project description:RNA-seq data from double positive thymocyte and CD4 or CD8 single positive spleen T cell

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Transcription profiling of thymocyte differentiation in knockout mouse models

Project description:Microarray experiment with whole thymi from genetically enginereed mice, with purified thymocyte samples and with cell lines.

2004-06-30 | E-MEXP-96 | biostudies-arrayexpress

RNA-seq of KMT2D Knockout and KMT2D WT melanoma in mice

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RNA-seq data from double positive thymocyte and CD4 or CD8 single positive spleen T cell

Project description:Control RNA-seq data for thymocyte and spleen T cell.

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DBC1 is a positive regulator of enhancer epigenomic writers KMT2D and p300.

Project description:DBC1 is a positive regulator of enhancer epigenomic writers KMT2D and p300.

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Epigenetic and transcriptional alterations with Kmt2c and Kmt2d knockout

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