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RNA-Seq shows the changes on transcriptomes after deletion of Nsd2 in KPC1199 cells.

ABSTRACT: To explore the possible role of Nsd2 in pancreatic carcinogenesis, the gene expression profile of Nsd2-WT and Nsd2-KO derived from KPC1199 cells was examined by RNA-seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE216562 | GEO | 2025/10/16

REPOSITORIES: GEO

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RNA-Seq shows the changes on transcriptomes after deletion of Nsd2 in KPC1199 cells.

Project description:RNA-Seq shows the changes on transcriptomes after deletion of Nsd2 in KPC1199 cells.

| PRJNA894221 | ENA

RNA-Seq shows the changes on transcriptomes after Nsd2 overexpression in mice.

Project description:To explore the possible role of Nsd2 in pancreatic carcinogenesis in vivo, the gene expression profile of pancreas tissue from PKNO(Pdx-Cre;LSL-KrasG12D;Nsd2oe/+) and littermate PK(Pdx-Cre;LSL-KrasG12D) mice (8 weeks old) was examined by RNA sequencing(RNA-Seq).

2025-10-13 | GSE215386 | GEO

Genome-wide maps of chromatin state in thymocytes from Nsd2-edited mice

Project description:We performed high-throughput profiling of histone modifications in mouse thymocytes in which Nsd2 were deleted (KO) or Nsd2 were substituted as following c.2717C>T; p.Pro906Leu that is an orthologous substitution of human NSD2 c.2714C>T; p.Pro905Leu (KI). We found that lysine 36 dimethylation were generally decreased in KO and KI. These were associated with regulation of gene expression.

2024-04-01 | GSE220890 | GEO

Epigenome analysis of wild type and Nsd2 gene-edited mice

Project description:Genome wide DNA methylation profiling of thymocytes from wild type and Nsd2 knock out (KO) and Nsd2 knock in (KI). The 906th Proline of Nsd2 was substituted to Leucine in Nsd2 KI by gene editing. The Illumina Infinium Mouse methylation Beadchip was used to obtain DNA methylation profiles across approximately 270,000 CpGs in thymocytes. Samples included 2 wild type, 2 heterozygous knock out, 1 heterozygous knock in, and 1 homozygous knock in.

2024-04-01 | GSE221621 | GEO

RNA-seq data from nsd2 wt and ko germinal center B cells

Project description:The goal of this study was to invetigate the mechanisms by which nsd2 regulate germinal center reaction by comparing RNA-seq data between nsd2 wt and ko germinal center B cells

2018-12-07 | GSE111755 | GEO

NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming

Project description:This SuperSeries is composed of the following subset Series: GSE29146: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [ChIP] GSE29147: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [RNAi] GSE29148: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [TKO] GSE29150: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [Transduction] Refer to individual Series

2011-11-29 | E-GEOD-29305 | biostudies-arrayexpress

NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [RNAi]

Project description:NSD2 (also named MMSET and WHSC1) is a histone lysine methyltransferase that is implicated in diverse diseases and commonly overexpressed in multiple myeloma due to a recurrent t(4;14) chromosomal translocation. However, the precise catalytic activity of NSD2 is obscure, preventing progress in understanding how this enzyme influences chromatin biology and myeloma pathogenesis. Here we show that dimethylation of histone H3 at lysine 36 (H3K36me2) is the principal chromatin-regulatory activity of NSD2. Catalysis of H3K36me2 by NSD2 is sufficient for gene activation. In t(4;14)-positive myeloma cells, the normal genome-wide and gene-specific distribution of H3K36me2 is obliterated, creating a chromatin landscape that selects for a transcription profile favorable for myelomagenesis. Catalytically active NSD2 confers xenograft tumor formation and invasion capacity upon t(4;14)-negative cells and NSD2 promotes oncogenic transformation of primary cells in an H3K36me2-dependent manner. Together our findings establish H3K36me2 as the primary product generated by NSD2, and demonstrate that genomic disorganization of this canonical chromatin mark initiates oncogenic programming. Genome-wide expression profiling of KMS11 cells stably transduced with control vector in comparison to two independent shRNAs against NSD2. Each cell line is tested in duplicate.

2011-11-29 | E-GEOD-29147 | biostudies-arrayexpress

NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [Transduction]

Project description:NSD2 (also named MMSET and WHSC1) is a histone lysine methyltransferase that is implicated in diverse diseases and commonly overexpressed in multiple myeloma due to a recurrent t(4;14) chromosomal translocation. However, the precise catalytic activity of NSD2 is obscure, preventing progress in understanding how this enzyme influences chromatin biology and myeloma pathogenesis. Here we show that dimethylation of histone H3 at lysine 36 (H3K36me2) is the principal chromatin-regulatory activity of NSD2. Catalysis of H3K36me2 by NSD2 is sufficient for gene activation. In t(4;14)-positive myeloma cells, the normal genome-wide and gene-specific distribution of H3K36me2 is obliterated, creating a chromatin landscape that selects for a transcription profile favorable for myelomagenesis. Catalytically active NSD2 confers xenograft tumor formation and invasion capacity upon t(4;14)-negative cells and NSD2 promotes oncogenic transformation of primary cells in an H3K36me2-dependent manner. Together our findings establish H3K36me2 as the primary product generated by NSD2, and demonstrate that genomic disorganization of this canonical chromatin mark initiates oncogenic programming. Genome-wide expression profiling of p19ARF-/- mouse embryonic fibroblasts stably transduced with control vector or wild-type NSD2. Each cell line is tested in triplicate.

2011-11-29 | E-GEOD-29150 | biostudies-arrayexpress

ATAC-seq analysis in KPC1199 murine PDAC cell line with or without glutamine starvation

Project description:We determined if up- and/or down-regulated genes in pancreatic tumor cells cultured under low-glutamine conditions were accompanied by alterations in genome-wide chromatin accessibility and then performed ATAC-seq of KPC1199 cells treated with low glutamine concentrations versus normal-media-treated controls. The ATAC-seq was performed according to the TruePrep Tagment Enzyme for ATACseq kit (TD501, Vazyme). DNA libraries were constructed following the manufacturer’s instructions of the Trueprep index kit v2 (TD202, Vazyme) and thereafter sequenced to an average of 20 million reads per sample.

2024-04-30 | GSE229051 | GEO

NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [TKO]

Project description:NSD2 (also named MMSET and WHSC1) is a histone lysine methyltransferase that is implicated in diverse diseases and commonly overexpressed in multiple myeloma due to a recurrent t(4;14) chromosomal translocation. However, the precise catalytic activity of NSD2 is obscure, preventing progress in understanding how this enzyme influences chromatin biology and myeloma pathogenesis. Here we show that dimethylation of histone H3 at lysine 36 (H3K36me2) is the principal chromatin-regulatory activity of NSD2. Catalysis of H3K36me2 by NSD2 is sufficient for gene activation. In t(4;14)-positive myeloma cells, the normal genome-wide and gene-specific distribution of H3K36me2 is obliterated, creating a chromatin landscape that selects for a transcription profile favorable for myelomagenesis. Catalytically active NSD2 confers xenograft tumor formation and invasion capacity upon t(4;14)-negative cells and NSD2 promotes oncogenic transformation of primary cells in an H3K36me2-dependent manner. Together our findings establish H3K36me2 as the primary product generated by NSD2, and demonstrate that genomic disorganization of this canonical chromatin mark initiates oncogenic programming. Genome-wide expression profiling of KMS11 and t(4;14) translocation knockout (TKO) cells. Each cell line is tested in triplicate.

2011-11-29 | E-GEOD-29148 | biostudies-arrayexpress

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