This SuperSeries is composed of the SubSeries listed below.
Ras dexamethasone-induced protein 1 is a modulator of hormone secretion in the volume overloaded heart.
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View SamplesThis SuperSeries is composed of the SubSeries listed below.
Functional analysis of the TRIB1 associated locus linked to plasma triglycerides and coronary artery disease.
Cell line
View SamplesPharmacological and gene ablation studies have demonstrated a crucial role of the caridac natriuretic peptides (NP) hormones ANF and BNP in the maintenance of cardiovascular homeostasis. Considerable effort has been focused on the elucidation of the mechanistic underlying increased atrial ANF and BNP expression and secretion. These investigations are important because under chronic congestive heart failure, the secretion of NPs although increased and beneficial, is relatively insufficient as demonstrated by the fact that patients benefit form the unloading of the heart induced by therapeutic administration of either ANF or BNP.
Ras dexamethasone-induced protein 1 is a modulator of hormone secretion in the volume overloaded heart.
No sample metadata fields
View SamplesPharmacological and gene ablation studies have demonstrated a crucial role of the caridac natriuretic peptides (NP) hormones ANF and BNP in the maintenance of cardiovascular homeostasis. Considerable effort has been focused on the elucidation of the mechanistic underlying increased atrial ANF and BNP expression and secretion. These investigations are important because under chronic congestive heart failure, the secretion of NPs although increased and beneficial, is relatively insufficient as demonstrated by the fact that patients benefit form the unloading of the heart induced by therapeutic administration of either ANF or BNP.
Ras dexamethasone-induced protein 1 is a modulator of hormone secretion in the volume overloaded heart.
No sample metadata fields
View SamplesTransfection experiments aimed at understanding the impact of upregulating lncRNA RP11-326A19.4 on the transcriptome; follow-up of GSE132451
<i>CARMAL</i> Is a Long Non-coding RNA Locus That Regulates <i>MFGE8</i> Expression.
Specimen part
View SamplesPharmacological and gene ablation studies have demonstrated a crucial role of the cardiac natriuretic peptides (NP) hormones ANF and BNP in the maintenance of cardiovascular homeostasis. In addition, hypertension and chronic congestive heart failure are clinical entities that may be regarded as states of relative NP deficiency. Hence the study of the function of the endocrine heart is highly relevant.
Transcriptional analysis of the mammalian heart with special reference to its endocrine function.
Sex, Specimen part
View SamplesDeletion experiment aimed at understanding the role of lncRNA RP11-326A19.4 /CARMAL via its deletion. The impact on of the deletion on the transcriptome was assessed by array analysis.
<i>CARMAL</i> Is a Long Non-coding RNA Locus That Regulates <i>MFGE8</i> Expression.
Specimen part
View SamplesThe TRIB1 locus has been associated with lipid dysfunction. The underlying mechanisms were investigated by examining the transcription landscape in response to TRIB1 suppression in human primary hepatocytes.
No associated publication
Specimen part
View SamplesObjective - The TRIB1 locus has been linked to hepatic triglyceride metabolism in mice and to plasma triglycerides and coronary artery disease (CAD) in humans. The lipid associated SNPs identified by genome-wide association studies (GWAS) are located ~ 30 kb downstream from TRIB1 suggesting complex regulatory effects on genes or pathways relevant to hepatic triglyceride metabolism. The goal of this study was to investigate the functional relationship between common SNPs at the TRIB1 locus and plasma lipid traits.
Functional analysis of the TRIB1 associated locus linked to plasma triglycerides and coronary artery disease.
Cell line
View SamplesThe NS1 protein of influenza A virus (IAV) is a multifunctional virulence factor. Mouse adaptive mutations in the NS1 protein of the human isolate A/Hong Kong/1/1968(H3N2) (HK) have been previously reported to increase virulence, viral fitness, and interferon antagonism, but differ in binding to post-transcriptional processing factor CPSF30. Because nuclear trafficking is a major genetic determinant of influenza virus host adaptation, we assessed subcellular localization and host gene expression of NS1 adaptive mutations. Recombinant HK viruses with adaptive mutations in the NS1 gene were assessed for NS1 protein subcellular localization in mouse and human cells using confocal microscopy and cellular fractionation. HK-wt virus NS1 partitioned equivalently between the cytoplasm and nucleus in human cells but was defective in cytoplasmic localization in mouse cells. The adaptive mutations either increased the proportion or abundance of NS1 in the cytoplasm, and/or the nucleus. NS1 mutations that increased cytoplasmic distribution identified a putative second nuclear export signal (NES) spanning aa positions 98-106 LSEDWFMLM, (mutation sites in bold); with the strongest effect seen for mutation M106I. The putative NES in the NS3 protein was associated with cytoplasmic localization. The host gene expression profile of the adaptive mutants was determined by microarray analysis of infected mouse cells to show either high or low gene regulation (HGR or LGR) phenotypes that mapped to the amino-terminal and the carboxy-terminal regions respectively. The HGR and LGR mutations were predominantly down regulating versus up regulating respectively. The greatest effect on host gene expression in the HGR group correlated with the ability of the NS1 protein to bind CPSF30. To our knowledge this is the first report of roles of adaptive NS1 mutations that affect intracellular localization and regulation of host gene expression.
Identification of adaptive mutations in the influenza A virus non-structural 1 gene that increase cytoplasmic localization and differentially regulate host gene expression.
Specimen part, Cell line
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