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Effect of depletion of KMT2C on gene expression in psoriasiform keratinocytes

ABSTRACT: Effect of depletion of KMT2C on gene expression in psoriasiform keratinocytes

PROVIDER: PRJNA832668 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18936964_1.fastq.gz	Fastqsanger.gz
	SRR18936964_2.fastq.gz	Fastqsanger.gz
	SRR18936965_1.fastq.gz	Fastqsanger.gz
	SRR18936965_2.fastq.gz	Fastqsanger.gz
	SRR18936966_1.fastq.gz	Fastqsanger.gz

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Effect of depletion of KMT2C on gene expression in psoriasiform keratinocytes

Project description:To investigate the function KMT2C in the psoriasis, we established M5(IL-17A, IL-22, oncostatin M, IL-1α, and TNF-α)-induced Ker-CT cell line in which has been knocked down by siKMT2C or contol. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells.

2022-04-30 | GSE201676 | GEO

IL-12 regulates type 3 immunity through interfollicular keratinocytes in psoriasiform inflammation

Project description:Psoriasis is a chronic inflammatory skin disorder underpinned by dysregulated cytokine signaling. Drugs neutralizing the common p40 subunit of IL-12 and IL-23 represented a therapeutic breakthrough; however, new drugs that block the IL-23p19 subunit and spare IL-12 are more effective, suggesting a regulatory function of IL-12. In order to pinpoint the cell type and underlying mechanism of IL-12 mediated immune-regulation in psoriasis we generated a conditional Il12rb2-knockout (KO)/reporter mouse strain. We detected Il12rb2 expression in T cells and a specific subset of interfollicular (IF) keratinocytes. Analysis of scRNAseq data from psoriasis patients confirmed this expression pattern in the human skin. Mechanistically, deletion of Il12rb2 in the keratinocyte compartment led to exacerbated psoriasiform inflammation. Protective IL-12 signaling blocked the hyperproliferation of keratinocytes, maintained skin barrier integrity, and, importantly, diminished disease-driving IL-23/type 3 immune circuits. Collectively, we provide a potential explanation for the superior efficacy of IL-23p19 inhibitors in psoriasis and describe an unperceived role of IL-12 in maintaining skin epithelial cell homeostasis.

2021-08-03 | GSE163700 | GEO

IL-12 regulates type 3 immunity through interfollicular keratinocytes in psoriasiform inflammation

Project description:IL-12 regulates type 3 immunity through interfollicular keratinocytes in psoriasiform inflammation

| PRJNA687223 | ENA

Aberrant downstream mechanisms following loss of KMT2C and KMT2D in Pancreatic Ductal Adenocarcinoma

Project description:Genes encoding the histone H3 lysine 4 (H3K4) methyltransferases KMT2C and KMT2D are subject to deletion and mutation in pancreatic ductal adenocarcinomas (PDAC). We examined the functional and transcriptional consequences of loss of these methyltransferases in patients with PDAC. Patients with low KMT2C and KMT2D expression demonstrated a much-improved outcome compared with those expressing high levels. RNA-seq analysis of KMT2C or KMT2D loss in three cell lines (PANC1, SUIT2 and COLO357) identified 31 and 124 differentially expressed genes respectively, with 19 genes common to both methlytransferases. Gene set enrichment analysis, and correlation with publicly available patient gene expression (GEP) datasets, highlighted significant reductions in pathways relating to cell-cycle and cell growth, where gene expression correlated with KMT2C/D depletion. Furthermore, loss of Kmt2d in three murine cell lines increased sensitivity to the nucleoside analogue 5-fluorouracil (5FU). These experiments support critical, non-redundant, roles for KMT2D and KMT2C in PDAC, where depletion impacts cell-cycle to reduce cell proliferation, enhance response to specific chemotherapy, which may improve patient survival.

2016-07-09 | GSE75327 | GEO

Effect of depletion of AIM2 on gene expression in psoriatic NETs-treated primary human keratinocytes

Project description:Effect of depletion of AIM2 on gene expression in psoriatic NETs-treated primary human keratinocytes

| PRJNA894149 | ENA

Synthesis and activity of the salicylic acid ester of bakuchiol in psoriasiform keratinocytes and skin substitutes

Project description:Background: Topical retinoids are effective in retarding skin aging and restoring homeostasis in skin conditions, such as psoriasis. However their adverse effects, which include irritation (retinoid dermatitis), photosensitivity and teratogenicity, limit their use level and patient compliance. Development of a retinoid analogue with minimal adverse effects would allow a broader and more compliant use. Objective: Here we report the synthesis of a novel molecule - bakuchiol salicylate (bakusylan) with the gene expression modulatory profile similar to retinoids, using as reference 3 prescription retinoids - tretinoin, tazarotene and adapalene. Methods: Having a structure entirely different from existing retinoids, we hypothesized that at least a partial uncoupling of retinoid adverse effects from retinoid skin normalizing activity may be obtained with bakuchiol salicylate. This hypothesis was tested in psoriasiform cultures of keratinocytes and organotypic skin substitutes by DNA microarrays and custom PCR arrays. Results: The evaluation of the bioactivity of bakuchiol salicylate revealed the elimination of several components of the retinoid-like proinflammatory response and teratogenic signature without a substantial loss of normalizing potential. A possible mechanism of action consisting in keratinocyte desensitization to cytokine signaling through the inhibition of the STAT1/3/interferon inflammatory signal transduction axis has also been identified. Conclusion: Bipartite materials obtained by merging two skin-active entities with specific, complementary bioactivities, such as bakuchiol and salicylic acid, may deliver a new class of functional retinoids.

2017-03-24 | GSE79642 | GEO

Effect of iASPP knockout in mouse keratinocytes

Project description:Effect of iASPP knockout in mouse keratinocytes

| PRJNA778802 | ENA

KMT2C methyltransferase domain regulated INK4A expression suppresses prostate cancer metastasis

Project description:Frequent truncating mutations of the histone lysine N‑methyltransferase KMT2C have been detected by whole exome sequencing studies in various cancers, including malignancies of the prostate. However, the biological consequences of these alterations in prostate cancer have not yet been elucidated. To investigate the functional impact of these mutations we deleted the C-terminal catalytic core motif of KMT2C specifically in the prostate epithelium of mice. We show here that impaired KMT2C methyltransferase activity drives proliferation and, when combined with loss of the tumour suppressor PTEN, triggers metastatic dissemination and reduces life expectancy. In our model system and human prostate cancer samples we show that KMT2C-mutated tumours activate the proliferative MYC signalling axis and fail to express the oncogene-induced cell cycle repressor p16INK4A. In addition, we observe a striking reduction in disease-free survival of patients with KMT2C-mutated prostate cancer. Thus, we identify truncated KMT2C as a driver of aggressive prostate cancer.

2022-05-02 | GSE186413 | GEO

Epigenetic and transcriptional alterations with Kmt2c and Kmt2d knockout

Project description:KMT2C and KMT2D are two of the most frequently mutated genes in bladder cancer and in histologically normal urothelium. In this study, we developed mouse models to investigate the molecular mechanism of Kmt2c/d loss in urothelial tumorigenesis.

2024-08-09 | GSE264514 | GEO

mRNA expression data from keratinocytes with disorganized lipid raft structures (by cholesterol depletion by methyl-beta-cyclodextrin)

Project description:Lipid rafts are cholesterol-rich cell signaling platforms and their physiological role can be explored by cholesterol depletion. To dress a global picture of transcriptional changes ongoing after lipid raft disruption, we performed whole-genome expression profiling in epidermal keratinocytes, a cell type which synthesizes its cholesterol in situ. We used microarrays to identify transcriptional changes in gene expression of cholesterol-depleted keratinocytes. Cholesterol depletion by methyl-beta-cyclodextrin disrupts the organization of lipid rafts, which are cholesterol- and sphingolipid-rich membrane microdomains. Transcript levels were measured in autocrine confluent cultures of normal human epidermal keratinocytes were either left untreated (Ctrl), cholesterol-depleted for 1h with 7.5mM methyl-beta-cyclodextrin (MBCD), or mock cholesterol-depleted for 1h with 7.5mM cholesterol-charged methyl-beta-cyclodextrin complexes (MBCD/chol) (Mock cholesterol depletion is a suppementary negative control as this treatment does not extract cholesterol from cell membranes). Samples are analysed either immediately after the treatment (R0h) or after recovery times of 1h (R1h) respectively 8h (R8h). in total 9 samples are analysed and no replicates are performed.

2010-04-17 | E-GEOD-21364 | biostudies-arrayexpress

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