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The effects of SCAP deletion on gene expression of activated B cells

ABSTRACT: The effects of SCAP deletion on gene expression of activated B cells

PROVIDER: PRJNA842708 | ENA |

REPOSITORIES: ENA

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The expression profiling comparison of mice with Scap and Insig deletion from perinatal lung (E17.5-PN1)

Project description:In this study, we studied the genomic responses of the Insig and Scap deletion from perinatal lung. Through comprehensive data analysis and integration, time dependent effects of epithelial SCAP/INSIG/SREBP deletion and defined SCAP/INSIG/SREBP-associated genes, bioprocesses and downstream pathways were identified. Total lung RNA was isolated from Scapdelata/delta, Insig1/2delta/delta, and respective control littermates at E17.5, E18.5 and PN1 were used for mRNA expression profiling analysis (n=3 for each condition)

2014-07-10 | E-GEOD-53397 | biostudies-arrayexpress

The effects of SCAP deletion on gene expression of activated B cells

Project description:To investigate the role of SREBP signaling in B cell activation, we stimulated SCAP+/+CD19Cre/+ (WT) and SCAPfl/fl CD19Cre/+ (KO) B cells with LPS, anti-CD40 or anti-IgM for 24 hrs and performed RNA sequencing to identifiy the differences.

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The expression profiling comparison of mice with Scap and Insig deletion from perinatal lung (E17.5-PN1)

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Deletion of Scap in Alveolar Type II Cells Influences Lung Lipid Homeostasis and Identifies a Compensatory Role for Pulmonary Lipofibroblasts

Project description:Pulmonary function after birth is dependent upon surfactant lipids that reduce surface tension in the alveoli. The sterol-responsive element-binding proteins (SREBPs) are transcription factors regulating expression of genes controlling lipid homeostasis in many tissues. To identify the role of SREBPs in the lung, we conditionally deleted the SREBP cleavage-activating protein gene, Scap, in respiratory epithelial cells (Scap∆/∆) in vivo. Prior to birth (E18.5), deletion of Scap decreased the expression of both SREBPs and a number of genes regulating fatty acid and cholesterol metabolism. Nevertheless, Scap∆/∆ mice survived postnatally, surfactant and lung tissue lipids being substantially normalized in adult Scap∆/∆ mice. Although phospholipid synthesis was decreased in type II cells from adult Scap∆/∆ mice, lipid storage, synthesis, and transfer by lung lipofibroblasts were increased. mRNA microarray data indicated that SCAP influenced two major gene networks, one regulating lipid metabolism and the other stress-related responses. Deletion of the SCAP/SREBP pathway in respiratory epithelial cells altered lung lipid homeostasis and induced compensatory lipid accumulation and synthesis in lung lipofibroblasts. To identify the role of SREBPs in the lung, we conditionally deleted the SREBP cleavage-activating protein gene, Scap, in respiratory epithelial cells (Scap∆/∆) in vivo.Lung cRNA was hybridized to the murine genome MOE430 V2 chips.

2011-01-08 | E-GEOD-26496 | biostudies-arrayexpress

Deletion of Scap in Alveolar Type II Cells Influences Lung Lipid Homeostasis and Identifies a Compensatory Role for Pulmonary Lipofibroblasts

2011-01-08 | GSE26496 | GEO

Liver gene expression profile of wild type, liver-specific PTEN KO, SCAP KO and PTEN/SCAP double KO mice.

Project description:Nonalcoholic steatohepatitis (NASH), a severe form of nonalcoholic fatty liver disease, is characterized by hepatic steatosis and hepatocellular injury and progresses to cirrhosis and hepatocellular carcinoma. Sterol regulatory element-binding proteins (SREBPs) are master regulators of lipogenesis. Liver-specific PTEN knockout (KO) mice show constitutive upregulation of SREBP through PI3K-Akt pathway activation, leading to spontaneous fatty liver and subsequent HCC development. SREBP cleavage-activating protein (SCAP) plays a critical role in SREBP activation. We sought to determine the impact of SREBP inhibition on NASH and HCC development. To this end, we additionally inhibited SREBP pathway in liver-specific PTEN mice by ablating SCAP and generated liver-specific PTEN/SCAP double KO (DKO) mice. However unexpectedly, inhibition of SCAP/SREBP pathway markedly exacerbated liver injury (5weeks), fibrosis (5months), and carcinogenesis (7 months) in PTEN KO mice. To elucidate the mechanisms of liver injury in liver-specific PTEN/SCAP DKO mice, we conducted transcriptome analyses of the livers.

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Impact of a pro-inflammatory stimulus on the miRNA composition of extracellular vesicles (EV) from stem cells from apical papilla (SCAP)

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Liver tumor gene expression profile of liver-specific PTEN KO, PTEN/SCAP double KO mice

Project description:Nonalcoholic steatohepatitis (NASH), a severe form of nonalcoholic fatty liver disease, is characterized by hepatic steatosis and hepatocellular injury and progresss cirrhosis and hepatocellular carcinoma. Sterol regulatory elment-binding proteins (SREBPs) are master regulators of lipogenesis. Liver-specific PTEN knockout (KO) mice show constitutive upregulation of SREBP through PI3K-Akt pathway activation, leading to spontaneous fatty liver and subsequent HCC development. SREBP cleavage-activating protein (SCAP) plays a critical role in SREBP activation. We sought to determine the impact of SREBP inhibition on NASH and HCC development. To this end, we additionaly inhibited SREBP pathway in liver-specific PTEN mice by ablating SCAP and generated liver-specific PTEN/SCAP double KO (DKO) mice. However unexpectedly, inhibition of SCAP/SREBP pathway markedly exacerbated liver injury (5weeks), fibrosis (5months), and carcinogenesis (7 months) in PTEN KO mice. To elucidate the mechanisms of liver tumorigenesis in liver-specific PTEN/SCAP DKO mice, we conducted transcriptome analyses of the livers.

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Gene expression data from mouse CD8 T cells

Project description:Determing the influence of lipid metabolism on murine T cell blastogenesis. Gene expression studies from purified spleen and lymph node T cells with conditional deletion of the SREBP Cleavage Activating Protein (SCAP) ex vivo or activated with plate-bound anti-CD3 and CD28 antibodies for 6 h. CD8 T cells were purified from T cell specific Scap deficient mouse spleens (KO, n=3) and control littermate (WT, n=3). The cells from each mouse were used for RNA extraction at either quiescent (T0) or 6 h activation (T6).

2013-02-13 | E-GEOD-44261 | biostudies-arrayexpress

Transcriptional Profliing of small molecules induced endothelial cells of stem cells from apical papilla (SCAP-ECs), stem cells from apical papilla (SCAP) and human vein endothelial cells (HUVECs)

Project description:Recently, a new strategy has been developed to directly reprogram one cell type towards targeted cell type by using different combinations of small molecule compounds. Here we attempted to induce stem cells from apical papilla (SCAP) into endothelial cells (ECs) by the same strategy. We developed a set of small molecules and growth factors that facilitates the conversion of SCAP into stable endothelial lineage. The SCAP-derived endothelial cells (SCAP-ECs) expressed some up-regulated endothelial specific genes and proteins, exhibited the ability to form functional tubular-like structures in vitro, and contributed to generate blood vessels in vivo. The aim of this study is to compare the ECs-related gene profile of SCAP, SCAP-derived ECs and HUVECs (primary ECs) and to explore whether SCAP-derived ECs showed enriched ECs gene expression.

2021-12-31 | GSE149930 | GEO

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