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RNAseq in LSD1 mouse stem cell models

ABSTRACT: RNAseq in LSD1 mouse stem cell models

PROVIDER: PRJEB77212 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR13344460_1.fastq.gz	Fastqsanger.gz
	ERR13344460_2.fastq.gz	Fastqsanger.gz
	ERR13344461_1.fastq.gz	Fastqsanger.gz
	ERR13344461_2.fastq.gz	Fastqsanger.gz
	ERR13344462_1.fastq.gz	Fastqsanger.gz

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RNAseq in LSD1 mouse stem cell models

Project description:Gene expression during in different LSD1 (KO, recovery, catalitically-inert) stem cell models in mice, in order to determine its molecular function

2024-07-16 | E-MTAB-14221 | biostudies-arrayexpress

Genome-wide map of lysine specific demethylase 1 (LSD1) in mouse embryonic stem cells.

Project description:We report the identification of LSD1 binding genomic regions in mouse embryonic stem cells (ESC) by high throughput sequencing. By obtaining over 10 million 36 bp reads of sequence from each chromatin immunoprecipitated DNA, we generated genome-wide maps for LSD1 and histone H3 dimethylated on lysine 4 (H3K4me2), the substrate for LSD1 in mouse ESCs. Our results showed an extensive overlap between the LSD1 and H3K4me2 genomic regions and a correlation between the genomic levels of LSD1/H3K4me2 and gene expression, including many highly expressed ESC genes. LSD1 is recruited to the chromatin of cells in the G1/S/G2 phases and is displaced from the chromatin of M phase cells, suggesting that LSD1 or H3K4me2 alternatively occupies LSD1 genomic regions during cell cycle progression. LSD1 knockdown by RNA interference or its displacement from the chromatin by anti-neoplastic agents caused an increase in the levels of a subset of LSD1 target genes. Taken together, these results suggest that cell-cycle dependent association and dissociation of LSD1 with chromatin mediates short-time scale gene expression changes during ES cell cycle progression. Examination of LSD1 and lysine 4 dimethylated histone H3 (H3K4me2) binding genomic regions in embryonic stem cells. Input genomic DNA and DNA immunoprecipitaed with control IgG was included as controls.

2012-10-03 | E-GEOD-18515 | biostudies-arrayexpress

Targeting Histone Demethylase LSD1 for Treatment of Deficits in Autism Mouse Models [RNA-seq]

Project description:We performed RNAseq experiments to examine genome-wide transcriptional changes in PFC of Shank3 +/∆C mice with or without GSK-LSD1 treatment.

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Bulk RNAseq of Basal Cell Carcinoma (BCC) mouse models

Project description:Bulk RNAseq of Basal Cell Carcinoma (BCC) mouse models

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Targeting Histone Demethylase LSD1 for Treatment of Deficits in Autism Mouse Models

Project description:Targeting Histone Demethylase LSD1 for Treatment of Deficits in Autism Mouse Models

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Genome-wide map of lysine specific demethylase 1 (LSD1) in mouse embryonic stem cells.

2012-10-03 | GSE18515 | GEO

LSD1 inhibtion in NEPC cell line models.

Project description:LSD1 inhibtion in NEPC cell line models.

| PRJNA906527 | ENA

LSD1 interactome in Glioblastoma

Project description:Tumor-initiating cells (TICs) play a critical role in glioblastoma (GBM) maintenance being responsible for its heterogeneity and resistance to standard therapy. A step toward clinical translation includes GBM TIC targeting. Among the molecules tested for GBM treatment, are those targeting epigenetic modifiers. By using patient-derived TICs and xenograft orthotopic models, we identified Lysine-specific histone demethylase 1A (LSD1) as a potentially druggable target in GBM. LSD1-directed therapy by means of the selective, orally bioavailable and brain penetrant inhibitor DDP_38003 effectively impairs growth, stem-like features and tumorigenic potential of GBM TICs. Our findings point to LSD1 as a positive regulator of Activating Transcription Factor 4 (ATF4)-dependent response in all stress conditions arising during tumor growth and therapy. Thus, through the downregulation of either ATF4 and its adaptive genes, LSD1 targeting is likely a promising strategy to hit GBM TICs by counteracting the ATF4-mediated adaptation to stress.

2022-06-02 | PXD021429 | Pride

Lsd1 coordinates trophoblast development by retaining stem cells in their niche and directing cell fate

Project description:Stem cells reside in specific niches providing stemness-maintaining environments. Thus, the regulated migration from these niches is associated with differentiation onset. However, mechanisms retaining stem cells in their niche remain poorly understood. Here, we show that the epigenetic regulator lysine-specific demethylase 1 (Lsd1) organises the trophoblast niche of the early mouse embryo by coordinating migration and invasion of trophoblast stem cells (TSCs). Lsd1 deficiency leads to the depletion of the stem cell pool resulting from precocious migration of TSCs. Migration is induced by premature expression of the transcription factor Ovol2 that is repressed by Lsd1 in undifferentiated wild-type TSCs. Increasing Ovol2 levels suffices to recapitulate the migration phenotype. Furthermore, Lsd1-deficient TSCs exhibit a developmental bias towards cells of the syncytiotrophoblast and impaired spongiotrophoblast and trophoblast giant cell differentiation. In summary, we describe that the epigenetic modifier Lsd1 coordinates placental development by retaining TSCs in their niche and directing trophoblast differentiation. Mouse trophoblast stem cells (TSCs) were isoloated from a single conditional Lsd1-deficient mouse (Lsd1tm1SchM-CM-<le). Deletion of Lsd1 was induced eight days before the collection of RNA by addition of 0.2 M-BM-5M 4OH-tamoxife. Cells were isolated at successive stages of differentiation for total RNA extraction and hybridization on Affymetrix microarrays. To that end, we harvested cells at three time-points: before induction of differentiation (d0), two days after induction of differentiation (d2), and four days after induction of differentiation (d4). Three replicates (1, 2, 3) for control (-) and Lsd1-deficeint (+) cells were included for each differentiation stage.

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