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Transcriptome profiling of NE-4C cells and NE-4C cells with knockdown of Setdb1 by RNA-sequencing

ABSTRACT: Transcriptome profiling of NE-4C cells and NE-4C cells with knockdown of Setdb1 by RNA-sequencing

PROVIDER: PRJNA791301 | ENA |

REPOSITORIES: ENA

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Transcriptome profiling of NE-4C cells and NE-4C cells with knockdown of Setdb1 by RNA-sequencing

Project description:NE-4C is a mouse neural stem cell line used for study of neuronal differentiation. Setdb1 is an epigenetic modification factor responsible for catalyzing the histone modification H3K9me3. Transcription of Setdb1 gene is enriched in embryonic neural cells during vertebrate embryogenesis. Setdb1 is upregulated in cancer cells and promotes cancers. We found that knockdown of Setdb1 in NE-4C cells led to neuronal differentiation.

2022-06-30 | GSE192373 | GEO

Proteomic profile of NE-4C cells after radiofrequency elecromagnetic field exposure and sham-exposure

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Transcriptome profiling of HCT116 cells and HCT116 cells with knockdown of SETDB1 by RNA-sequencing

Project description:HCT116 is a colorectal cancer cell line. SETDB1 is an epigenetic modification factor responsible for catalyzing the histone modification H3K9me3. Transcription of SETDB1 gene is enriched in embryonic neural cells during vertebrate embryogenesis. SETDB1 is upregulated in cancer cells and promotes cancers. We found that knockdown of SETDB1 in HCT116 cells led to a neuronal-like differentiation phenotype.

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Identification of Setdb1 interaction proteins in neural stem cells

Project description:Setdb1 is an epigenetic factors catalyzing modification of H3K9me3. Expression of its gene is localized to embryonic neural cells during vertebrate embryogenesis, suggesting its role in regulating neural stemness. The project is to identify the interaction partners of Setdb1, by which Setdb1 regulates neural stemness in neural stem cells.

2022-08-12 | PXD030453 | Pride

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Setdb1-mediated H3K9 methylation is enriched on the inactive X and plays a role in its epigenetic silencing

Project description:Purpose: The aim of this study is (1) to identify the chromatin occupancy of the epigenetic regulator Setdb1 in mouse embryonic fibroblasts (MEF); (2) to profile key epigenetic marks H3K9me2, H3K9me3 and H3K27me3; utilizing wildtype cells with nonsilencing shRNA mediated knockdown and Setdb1 geneTrap heterozygous cells with Setdb1 shRNA mediated knockdown. Methods: Chromatin immunoprecipitation for Setdb1, H3K9me2, H3K9me3 and H3K27me3 was performed essentially as in (Nelson et al. 2006). Briefly, nuclei were isolated from formaldehyde crosslinked MEFs and chromatin was fragmented by sonication. Chromatin immunoprecipitation was performed with corresponding antibodies for Setdb1, H3K9me2, H3K9me3 and H3K27me3. DNA was extracted from the immunoprecipitated fraction following reverse-crosslinking. Isolated DNA was used to generate sequencing libraries with Illumina's TruSeq DNA Sample Preparation Kit according to manufacturer's instruction. Libraries were pooled and sequenced on the Illumina HiSeq 2000 platform for 100 bp single-end reads. Image analysis was performed in real time by the HiSeq Control Software (HCS) v1.4.8 and Real Time Analysis (RTA) v1.12.4.2, running on the instrument computer. Real-time base calling on the HiSeq instrument computer was performed with the RTA software. Illumina CASAVA1.8 pipeline was used to generate the sequence data. Chromatin occupancy of the epigenetic regulator Setdb1, H3K9me2, H3K9me3 and H3K27me3 in mouse embryonic fibroblasts (MEFs) with wildtype MEFs and nonsilencing shRNA mediated knockdown or Setdb1 geneTrap heterozygous MEFs with Setdb1 shRNA mediated knockdown was determined by Setdb1, H3K9me2, H3K9me3 and H3K27me3 ChIP-seq, respectively.

2016-05-18 | E-GEOD-66522 | biostudies-arrayexpress

Hypoxia stabilizes SETDB1 to maintain genome stability

Project description:Von Hippel-Lindau (VHL) is a tumor suppressor that functions as the substrate recognition subunit of the CRL2VHL E3 complex. While substrates of VHL have been identified, its tumor suppressive role remains to be fully understood. For further determination of VHL substrates, we analyzed the physical interactome of VHL and identified the histone H3K9 methyltransferase SETBD1 as a novel target. SETDB1 undergoes oxygen-dependent hydroxylation by prolyl hydroxylase domain proteins (PHD) and the CRL2VHL complex recognizes hydroxylated SETDB1 for ubiquitin-mediated degradation. Under hypoxic conditions, SETDB1 accumulates by escaping CRL2VHL activity. Loss of SETDB1 in hypoxia compared with that in normoxia escalates the production of transposable element (TE)-derived double-stranded RNAs (dsRNAs), thereby hyperactivating the immune-inflammatory response. In addition, strong derepression of TEs in hypoxic cells lacking SETDB1 triggers DNA damage-induced death. Our collective results support a molecular mechanism of oxygen-dependent SETDB1 degradation by the CRL2VHL E3 complex and reveal a role of SETDB1 in genome stability under hypoxia.

2024-01-26 | PXD037104 | Pride

Transcriptome profiling of HCT116 cells and HCT116 cells with knockdown of SETDB1 by RNA-sequencing

Project description:Transcriptome profiling of HCT116 cells and HCT116 cells with knockdown of SETDB1 by RNA-sequencing

| PRJNA791302 | ENA

Setdb1-mediated H3K9 methylation is enriched on the inactive X and plays a role in its epigenetic silencing

Project description:Purpose: The aim of this study was to determine the DNA methylation state of wildtype female mouse embryonic fibroblasts with nonsilencing shRNA mediated knockdown and Setdb1 geneTrap heterozygous cells with Setdb1 shRNA mediated knockdown. Methods: Enhanced Reduced Representation Bisulfite Libraries (eRRBS) were produced as previously descirbed (Akalin et al. 2012). Libraries were pooled and sequenced on the Illumina HiSeq 2000 platform for 100 bp single-end reads with dark cycle parameters (Boyle et al. 2012). Image analysis was performed in real time by the HiSeq Control Software (HCS) v1.4.8 and Real Time Analysis (RTA) v1.12.4.2, running on the instrument computer. Real-time base calling on the HiSeq instrument computer was performed with the RTA software. Illumina CASAVA1.8 pipeline was used to generate the sequence data. Determine the DNA methylation state of mouse embryonic fibroblasts (MEFs) with wildtype MEFs and nonsilencing shRNA mediated knockdown or Setdb1 geneTrap heterozygous MEFs with Setdb1 shRNA mediated knockdown. Single-end with dark cycle protocol (Boyle et al. 2012)

2016-05-18 | E-GEOD-66524 | biostudies-arrayexpress

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