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Transcriptome sequencing of differentially expressed genes of the skin tissue of Ncstn ΔKC mice and normal mice

ABSTRACT: Transcriptome sequencing of differentially expressed genes of the skin tissue of Ncstn ΔKC mice and normal mice

PROVIDER: PRJNA473793 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7235080_1.fastq.gz	Fastqsanger.gz
	SRR7235080_2.fastq.gz	Fastqsanger.gz
	SRR7235081_1.fastq.gz	Fastqsanger.gz
	SRR7235081_2.fastq.gz	Fastqsanger.gz
	SRR7235082_1.fastq.gz	Fastqsanger.gz

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Transcriptome sequencing of differentially expressed genes of the skin tissue of Ncstn ΔKC mice and normal mice

Project description:We constructed keratinocyte-specific Ncstn-knockout mice to investigate the role of NCSTN in the pathogenesis of human AI.

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transcriptome-wide map of NCSTN-KD and NC Hacat cells

Project description:Acne inversa (AI) is an inflammatory skin disease associated with the nicastrin (NCSTN) mutations. Family history with autosomal dominant inheritance has heen reported in AI patients and are associated with mutations in the γ-secretase subunit, nicastrin (NCSTN), presenilin enhancer 2 (PSENEN), and presenilin-1 (PSEN1). Among them, NCSTN gene has the highest mutation rate. To detect the impact of NCSTN deficiency on AI keratinocytes. Here, using the short hairpin RNA (shRNA)-mediated gene knockdown and RNA sequencing technology, we explored the differentially expressed genes regulated by NCSTN deficiency in HaCaT cells.

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Transcriptome sequencing of differentially expressed genes in acne inversa (AI) patients with NCSTN mutation and healthy individuals

Project description:To elucidate the relationship between NCSTN mutations and familial AI pathogenesis by investigating differential gene expression, we have employed transcriptome sequencing profiling as a discovery platform to identify genes with the potential to be involved in familial AI pathogenesis. Skin biopsies were obtained from the lesions of AI patients with NCSTN mutations . Control skin tissues were obtained from healthy individuals undergoing cosmetic surgery procedures

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Effects of nicastrin (NCSTN) siRNA knockdown in HEK293 and HEK001 cells.

Project description:The goal of this study was to determine if knockdown of nicastrin induced a proinflammatory phenotype in HEK001 and HEK293 cells. Nicastrin (NCSTN) is a member of the gamma-secretase complex, and has been identified as the most frequently mutated gene in familial hidradenitis suppurativa. While much research has been done into the effects of PSEN1 and PSEN2 loss, less is known about isolated NCSTN haploinsufficiency. Two cell lines were knocked down with either NCSTN siRNA or an siRNA to luciferase in triplicate. RNA was extracted from drug selected knockdowns and profiled on the Illumina Human HT-12 v4 beadarray. Gene ontology analysis of differentially expressed genes revealed a proinflammatory and decreased proliferation signature in keratinocytes. HEK293 cells demonstrated expression signatures for decreased cholesterol synthesis and interferon-alpha signaling, as well as increased p53 signaling and caspase mediated cytoskeletal cleavage. 12 total samples. Two cell lines (HEK001 & HEK293) each with two treatments (NCSTN siRNA knockdown or pLKO luciferase knockdown) in three parallel 3 replicates each. For each line gives the changes specific to knockdown of gamma-secretase component nicastrin (NCSTN).

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Transcriptome sequencing of differentially expressed genes in acne inversa (AI) patients with NCSTN mutation and healthy individuals

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Differentially expressed RNAs in the skin tissue of IRF1 knockout mice following radiation

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Effects of nicastrin (NCSTN) siRNA knockdown in HEK293 and HEK001 cells.

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