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PRMT1 and CSNK1a1 control epidermal progenitor maintenance (PRMT1/CSNK1a1 transcriptome profiling data sets)

ABSTRACT: PRMT1 and CSNK1a1 control epidermal progenitor maintenance (PRMT1/CSNK1a1 transcriptome profiling data sets)

PROVIDER: PRJNA432779 | ENA |

REPOSITORIES: ENA

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PRMT1 and CSNK1a1 control epidermal progenitor maintenance (PRMT1/CSNK1a1 transcriptome profiling data sets)

Project description:Here we determine the target gene sets controlled by PRMT1 or CSNK1a1 in maintaining the undifferentiated state of primary human keratinocytes.

2018-02-02 | GSE110049 | GEO

PRMT1 and CSNK1a1 control epidermal progenitor maintenance

Project description:PRMT1 and CSNK1a1 control epidermal progenitor maintenance

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PRMT1 and CSNK1a1 control epidermal progenitor maintanence (PRMT1 ChIP-seq data set)

Project description:PRMT1 and CSNK1a1 control epidermal progenitor maintanence (PRMT1 ChIP-seq data set)

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PRMT1 and CSNK1a1 control epidermal progenitor maintanence (PRMT1 ChIP-seq data set)

Project description:Here we determine the genome-wide binding sites of PRMT1 in primary human keratinocytes. We also investigated the impact of casein kinase inhibitor D4476 on PRMT1 genomic binding.

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PRMT1 and CSNK1a1 control epidermal progenitor maintenance

Project description:This SuperSeries is composed of the SubSeries listed below.

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Targeting epigenetic networks mediated by Prmt1 and Kdm4c in acute myeloid leukemia

Project description:Transcriptional deregulation plays a major role in acute myeloid leukemia, identification of epigenetic modifying enzymes essential for the maintenance of oncogenic transcription programs holds the key to better understanding the biology and designing effective therapeutic strategies for the disease. Here we provide experimental evidence showing the functional involvement and therapeutic potentials of targeting PRMT1 with H4R3 methyltransferase activity in various MLL and non-MLL leukemias. PRMT1 is necessary but not sufficient for leukemic transformation, which requires co-recruitment of KDM4C with H3K9 demethylase activity by chimeric transcription factors to mediate epigenetic reprogramming. Inhibition of KDM4C/PRMT1 suppresses transcription and transformation ability of MLL fusions and MOZ-TIF2, revealing a novel and targetable epigenetic circuitry mediated by PRMT1 and KDM4C in acute leukemia.

2016-01-14 | E-MTAB-3322 | biostudies-arrayexpress

PRMT1-mediated FLT3 arginine methylation is required for maintenance of FLT3-ITD+ Acute Myeloid Leukemia

Project description:The presence of FLT3-ITD mutations in patients with acute myeloid leukemia (AML) is associated with poor clinical outcome. FLT3 tyrosine kinase inhibitors (TKIs), although effective in kinase ablation, do not eliminate FLT3-ITD+ leukemia stem cells (LSCs) which are potential sources of disease relapse, prompting us to ask whether FLT3-ITD protein regulates the AML LSCs survival through a kinase-independent mechanism. Here, we show that expression of PRMT1, the primary type I arginine methyltransferase, significantly increases in LSC-enriched CD34+CD38- populations relative to normal counterparts. Genetic PRMT1 depletion blocked AML CD34+ cell survival, and had more potent effects in AML cells from patients harboring FLT3-ITD. Our genome wide analysis of gene expression and PRMT1 conditional KO mouse study confirmed that PRMT1 preferentially cooperates with FLT3-ITD contributing to AML cell maintenance. Mechanistically, PRMT1 catalyzed FLT3-ITD protein methylation at arginines 972/973, and PRMT1 promoted leukemia cell growth in a FLT3 methylation-dependent manner. Moreover, effects of FLT3-ITD methylation in AML cells were in part due to crosstalk with FLT3-ITD phosphorylation at tyrosine 969 (Y969). Importantly, FLT3 methylation persisted in FLT3-ITD+ AML cells following TKI (AC220) treatment, indicating that methylation occurs independently of kinase activity. Finally, in both patient-derived xenograft (PDX) and murine AML models, combined administration of AC220 with a type I PRMT inhibitor (MS023) enhanced elimination of FLT3-ITD+ AML relative to AC220 treatment alone. Our study demonstrates that PRMT1-mediated FLT3 methylation promotes LSC activity and suggests that combining PRMT1 inhibition with FLT3 TKI treatment could be a promising approach to selectively target FLT3-ITD+ LSCs.

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Project description:We found found that casein kinase 1 alpha (Csnk1a1), a serine threonine kinase and negative regulator of beta catenin, is essential for leukemia cells in vivo. We examined the effect of Csnk1a1 knowckdown by gene expression profiling in primary leukemia cells.

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Roles of ESRPs in maintenance of epidermal transcriptome

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