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Plasma and B cells from mice treated with GSK-LSD1

ABSTRACT: We treated mice daily with the GSK-LSD1 or vehicle for 21 days. B and plasma cells were isolated by FACS and RNA-seq performed. Pathway analysis showed that MYC targets, Unfolded protein response, TNFalpha signaling, STAT3, STAT5 and other signaling pathways were significantly altered.

ORGANISM(S): Mus musculus

PROVIDER: GSE85596 | GEO | 2017/08/12

SECONDARY ACCESSION(S): PRJNA338916

REPOSITORIES: GEO

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Human small intestinal organoids grown with a specific protocol to enrich for Paneth cells were treated with an inhbitor (GSK-LSD1) for the epigenetic modulator LSD1.

Project description:To assess the role of LSD1 in human intestinal epithelium, human small intestinal organoids were treated with an inhibitor for LSD1 (GSK-LSD1) and compared to untreated organoids. The organoids were grown with specific conditions where Paneth cells are present in the organoids as similar experiments in mice show that Paneth cells disappear upon GSK-LSD1 treatment. Similar to mouse intestinal organoids, Paneth cells dissappear upon GSK-LSD1 treatment. Furthermore, we used these gene set enrichment analysis on these microarray data to show that these human intestinal organoids have a similar phenotype as mice epithelium without LSD1.

2020-11-16 | E-MTAB-7863 | biostudies-arrayexpress

RNA-seq of small intestinal organoids treated with an inhibitor for the epigenetic modifier LSD1

Project description:To assess the role of LSD1 in mice small intestinal epithelium, small intestinal organoids were treated with an inhibitor for LSD1 (GSK-LSD1) and compared to untreated organoids. Similar to intestinal epithelium from mice with an intestinal epithelium specific LSD1-KO, paneth cells dissappear upon GSK-LSD1 treatment. We used these sequencing data to show that these small intestinal organoids have a similar phenotype as mice epithelium without LSD1.

2020-11-16 | E-MTAB-9077 | biostudies-arrayexpress

LSD1 pharmacological inhibition in SET-2 containing wild type and mutant LSD1 [ChIP-Seq]

Project description:We characterized the changes in histone modifications as well as the localization of LSD1 and GFI1B for both wt SET-2 and drug-resistant SET-2 LSD1 (Leu659_Asn660insArg) treated with GSK-LSD1

2019-01-23 | GSE121424 | GEO

LSD1 pharmacological inhibition in SET-2 containing wild type and mutant LSD1 [RNA-Seq]

Project description:We characterized the effect of GSK-LSD1 treatment on gene expression for both wt SET-2 and drug-resistant SET-2 LSD1 (Leu659_Asn660insArg)

2019-01-23 | GSE121425 | GEO

Systemic LSD1 inhibition prevents aberrant remodeling of metabolism in obesity

Project description:The transition from lean to obese states involves systemic metabolic remodeling that impacts insulin sensitivity, lipid partitioning, inflammation, and glycemic control. Here, we have taken a pharmacological approach to test the role of a nutrient-regulated chromatin modifier, lysine-specific demethylase (LSD1), in obesity-associated metabolic reprogramming. We show that systemic administration of an LSD1 inhibitor (GSK-LSD1) reduces food intake and body weight, ameliorates non-alcoholic fatty liver disease (NAFLD), and improves insulin sensitivity and glycemic control in mouse models of obesity. GSK-LSD1 has little effect on systemic metabolism of lean mice, suggesting LSD1 has a context-dependent role in promoting maladaptive changes in obesity. Analysis of insulin target tissues identified white adipose tissue as the major site of insulin sensitization by GSK-LSD1, where it reduces adipocyte inflammation and lipolysis. We demonstrate that GSK-LSD1 reverses NAFLD in a non-hepatocyte-autonomous manner, suggesting an indirect mechanism potentially via inhibition of adipocyte lipolysis and subsequent effects on lipid partitioning. Pair-feeding experiments further revealed that effects of GSK-LSD1 on hyperglycemia and NAFLD are not a consequence of reduced food intake and weight loss. These findings suggest that targeting LSD1 could be a strategy for treatment of obesity and its associated complications including type 2 diabetes and NAFLD.

2022-10-17 | GSE210761 | GEO

ChIP-seq analysis of gene expression regulated by LSD1 in CD8+ T cells

Project description:ChIP-seq assay was performed with GSK- or Vehicle-treated CD8+ T cells to interrogate the genome-wide distribution of LSD1, H3K4me1, H3K4me2, H3K4me3, H3K27ac, and Pol II, and their alterations in response to LSD1 inhibition.

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GFI1B and LSD1 repress myeloid traits during megakaryocyte differentiation

Project description:The transcription factor Growth Factor Independence 1B (GFI1B) recruits Lysine Specific Demethylase 1A (LSD1/KDM1A) to stimulate gene programs relevant for megakaryocyte and platelet biology. Inherited pathogenic GFI1B variants result in thrombocytopenia and bleeding propensities with varying intensity. Whether these affect similar gene programs is unknow. Here we studied transcriptomic effects of four patient-derived GFI1B variants (GFI1BT174N,H181Y,R184P,Q287*) in MEG01 megakaryoblasts. Compared to normal GFI1B, each variant affected different gene programs with GFI1BQ287* uniquely failing to repress myeloid traits. In line with this, single cell RNA-sequencing of induced pluripotent stem cell (iPSC)-derived megakaryocytes revealed a 4.5-fold decrease in the megakaryocyte/myeloid cell ratio in GFI1BQ287* versus normal conditions. Inhibiting the GFI1B-LSD1 interaction with small molecule GSK-LSD1 resulted in activation of myeloid genes in normal iPSC-derived megakaryocytes similar as observed for GFI1BQ287* iPSC-derived megakaryocytes. Thus, GFI1B and LSD1 facilitate gene programs relevant for megakaryopoiesis while simultaneously repressing programs that induce myeloid differentiation.

2024-03-28 | PXD050401 | Pride

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.

2022-01-13 | GSE193380 | GEO

RNA-seq data of esophageal cancer cell Kyse510 after inhibition or silencing of LSD1 and G9a

Project description:The goals of this study are to compare transcriptome profiling (mRNA level) and signaling pathways between the control and ablating LSD1, the control and ablating G9a, the control and co-ablating LSD1 and G9a. We found pathways in apoptosis, endoplasmic reticulum stress and unfolded protein response were obviously changed in these groups, which are important for esophageal cancer therapy.

2022-05-01 | GSE173666 | GEO

GSK-3A and GSK-3B knockdown in AML cell lines

Project description:Gene expression data from AML cell lines, MOLM-14, U937, THP-1 and HL-60, that were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), or two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6). Acute myeloid leukemia (AML) is the most common form of acute leukemia in adults. Long-term survival of patients with AML has changed little over the past decade, necessitating the identification and validation of new AML targets. Integration of genomic approaches with small-molecule and genetic-based high-throughput screening holds the promise of improved discovery of candidate targets for cancer therapy. Here, we identified a role for glycogen synthase kinase 3A (GSK-3A) in AML by performing two independent small-molecule library screens and an shRNA screen for perturbations that induced a differentiation expression signature in AML cells. GSK-3 is a serine-threonine kinase involved in diverse cellular processes including differentiation, signal transduction, cell cycle regulation, and proliferation. We demonstrated that specific loss of GSK-3A induced differentiation in AML by multiple measurements, including induction of gene expression signatures, morphological changes, and cell surface markers consistent with myeloid maturation. GSK-3AM-bM-^@M-^Sspecific suppression also led to impaired growth and proliferation in vitro, induction of apoptosis, loss of colony formation in methylcellulose, and anti-AML activity in vivo. Although the role of GSK-3B has been well studied in cancer development, these studies support a role for GSK-3A in AML. The AML cell lines, MOLM-14, U937, THP-1 and HL-60, were infected with a scrambled control hairpin (shControl), two shRNAs directed against GSK-3B (shGSK3B_1 and shGSK3B_2), and two shRNAs directed against GSK-3A (shGSK3A_5 and shGSK3A_6).

2012-02-27 | E-GEOD-35200 | biostudies-arrayexpress

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