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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE57949 | GEO | 2014/11/26

SECONDARY ACCESSION(S): PRJNA248473

REPOSITORIES: GEO

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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).

2014-11-26 | E-GEOD-57949 | biostudies-arrayexpress

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.

2023-12-31 | GSE209911 | GEO

Homo sapiens

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

| PRJNA248473 | ENA

RNA sequencing of skin punch biopsies of lesional and non-lesional skin from hidradenitis suppurativa patients

Project description:This study investigated the underlying inflammatory pathways and cell types in hidradenitis suppurativa using transcriptomic approaches with RNA sequencing of lesional and non-lesional skin biopsies from hidradenitis suppurativa patients.

2023-12-06 | GSE249027 | GEO

To investigate the alteration of gene expression profiles after NCSTN gene silencing in HaCaT cells employing Agilent whole genome microarray

Project description:The present study was designed to use small interfering RNA (siRNA) approach to identify the effects of NCSTN silencing on human immortal keratinocyte cell line, HaCaT. The alteration of gene expression profiles after NCSTN gene silencing in HaCaT cells was investigated employing Agilent whole genome microarray

2018-04-28 | GSE68346 | GEO

Alterations to the Hidradenitis Suppurativa Serum Proteome with Spleen Tyrosine Kinase Antagonism: Proteomic Results from a Phase 2 Clinical Trial.

Project description:Serum Proteomic Analysis of patients with Hidradenitis Suppurativa treated with Fostamatinib

2023-08-10 | GSE240607 | GEO

Gene expression profiling of blood in hidradenitis suppurativa

Project description:To acquire a better understanding of the molecular pathogenesis of hidradenitis suppurativa (HS), we performed mRNA microarray studies to compare whole blood gene expression of HS patients to that of healthy normal subjects. No significant difference was observed in whole blood mRNA expression between HS patients and healthy normal control. Whole blood samples were collected from patients with hidradenitis (n=16) at baseline and healthy normal subjects (n=10) for RNA extraction and microarray analysis.

2016-03-11 | E-GEOD-79149 | biostudies-arrayexpress

Expression data from LSK WT and LSK NcstnKO

Project description:Notch signaling is one of the central regulators of differentiation in a variety of organisms and tissue types. Within the hematopoietic system, Notch is essential for the emergence of definitive HSC during fetal life and controls adult HSC differentiation to the T-cell lineage. Notch activation is controlled by the gamma-secretase complex complex, composed of presenilin, nicastrin (Ncstn), anterior pharynx-1 (Aph1), and presenilin enhancer-2 To determine other role of Notch signaling in HSC we designed a conditional mouse model of Nicastrin deletion. WT and KO HSC were analysed to determined genes controlled by Notch signaling. Bone marrow lineage negative, cKit+, Sca1+ cells were sorted from WT and Ncstn KO littermates for RNA extraction and hybridization on Affymetrix microarrays

2011-05-12 | E-GEOD-27794 | biostudies-arrayexpress

Expression data from LSK WT, GMP WT and GMP NcstnKO

Project description:Notch signaling is one of the central regulators of differentiation in a variety of organisms and tissue types. Within the hematopoietic system, Notch is essential for the emergence of definitive HSC during fetal life and controls adult HSC differentiation to the T-cell lineage. Notch activation is controlled by the gamma-secretase complex complex, composed of presenilin, nicastrin (Ncstn), anterior pharynx-1 (Aph1), and presenilin enhancer-2 To determine other role of Notch signaling in HSC we designed a conditional mouse model of Nicastrin deletion. WT and KO HSC were analysed to determined genes controlled by Notch signaling. Bone marrow lineage negative, cKit+, Sca1+ and lineage negative, cKit+, Sca1- CD34+ FcgammaRII/III+ cells were sorted from WT and Ncstn KO littermates for RNA extraction and hybridization on Affymetrix microarrays

2011-05-12 | E-GEOD-27811 | biostudies-arrayexpress

A Hidradenitis Suppurativa Molecular Disease Signature Derived from Patient Samples by High-Throughput RNA Sequencing

Project description:Hidradenitis suppurativa is a common, debilitating inflammatory skin disease linked to immune dysregulation and abnormalities in follicular structure and function. Few studies have characterized the transcriptomic profile of affected and unaffected skin. We established an RNA-Seq based hidradenitis suppurativa expression disease signature and found it largely concordant with an earlier microarray-based study. We confirmed known aspects of the underlying disease biology including known immune response pathways, differential regulation of antimicrobial peptides, and complement activation. We further characterize the extent of changes in the complement cascade in hidradenitis lesions and highlight a signature that implicates host response to bacteria in disease pathogenesis.

2020-12-31 | GSE151243 | GEO

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