Adar1 is an essential gene for mouse embryonic development. Adar1 null mouse embryos dies around E11.5 because of massive apoptosis. Overall design: Small RNA: 4 samples examined: wild type E11.0, ADAR1 null E11.0, wild type E11.5, ADAR1 null E11.5, mRNA-seq: wild type E11.5, ADAR1 null E11.5.
ADAR1 forms a complex with Dicer to promote microRNA processing and RNA-induced gene silencing.
Specimen part, Cell line, Subject
View SamplesSmall RNA expression was analysed in total RNA of HeLa cells treated with siRNA toward Luciferase (negative cotrol) or ADAR1. Overall design: Small RNA: 2 samples examined: HeLa cell with siLuc (negative cotrol), with siADAR1
ADAR1 forms a complex with Dicer to promote microRNA processing and RNA-induced gene silencing.
Cell line, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Tbx3-dependent amplifying stem cell progeny drives interfollicular epidermal expansion during pregnancy and regeneration.
Sex, Specimen part
View SamplesTo identify genes expressed predominantly in the ventral skin epidermal basal cells of pregnant mice, we performed DNA microarray analysis by using FACS-purified epidermal basal cells from ventral skin at 0 and 16 dpc, and dorsal skin at 16 dpc.
Tbx3-dependent amplifying stem cell progeny drives interfollicular epidermal expansion during pregnancy and regeneration.
Sex, Specimen part
View SamplesTo identify genes expressed predominantly in the ventral skin dermis of pregnant mice, we performed DNA microarray analysis by using isolated dermal tissues from ventral skin at 0 and 15 dpc, PP2-injected ventral skin at 15 dpc, and dorsal skin at 15 dpc.
Tbx3-dependent amplifying stem cell progeny drives interfollicular epidermal expansion during pregnancy and regeneration.
Sex, Specimen part
View SamplesObjective: Adult Stills disease (ASD) is a systemic disorder of unknown etiology characterized by high spiking fever, rash and arthritis. The purpose of this study was to determine the pathogenic roles of specific genes in ASD. Methods: Differentially expressed genes (DEGs) were examined by DNA microarray and validated by quantitative PCR using monocytes isolated from patients with active-ASD, inactive-ASD and healthy controls. The correlation between validated DEGs and ASD activity was analyzed. After inflammasome activation with LPS and Nigericin, the production of IL-1, IL-18, inflammasome and autophagy related proteins in DEGs-overexpressing THP-1 cells was carried out by ELISA or western blotting. DEGs-overexpressing THP-1 cells were treated with an inhibitor of autophagy followed by assessment of IL-1 and IL-18 production by ELISA and western blotting method.Conclusions: The overexpression of PLAC8 in monocytes might play a regulatory role in the production of IL-1 and IL-18 by the enhancement of autophagy, resulting in the suppression of ASD. Results:A total of 68 genes were highly expressed in monocytes isolated from active-ASD patients, relative to their expression in inactive-ASD patients and healthy controls. After validation of expression of 13 genes (CLU, FCGR1B, PLAC8, TLR1, S100A12, CD55, PIM1, BCL2A1, SOD2, PLSCR1, CYP1B1, STEAP4, IL1RN), the expression of PLAC8 was significantly higher in active-ASD patients than the other groups. In ASD, PLAC8 expression level correlated with serum levels of CRP, ferritin and IL-18. Stimulation of monocytes with lipopolysaccharide resulted in PLAC8 upregulation. LPS or Nigericin stimulation of PLAC8-overexpressing THP-1, but not THP-1 cells< was associated with significant decrease in IL-1 and IL-18 production. PLAC8 overexpressing in THP-1 cells was associated with enhanced autophagy and suppression of IL-1 and IL-18 production. Conclusions: PLAC8 upregulation in monocytes seemed to play a regulatory role in the production of IL-1 and IL-18 through enhanced autophagy, resulting in suppression of ASD. The results highlight the role of PLAC8 in the pathogenesis of ASD and suggest its potential suitability as a therapeutic target in ASD.
Placenta Specific 8 Suppresses IL-18 Production through Regulation of Autophagy and Is Associated with Adult Still Disease.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesAlthough microbiota plays a critical role for the normal development and function of host immune systems, the detail of the influence, especially on those in the large intestine (LI), remains unknown.
Importance of the interferon-alpha system in murine large intestine indicated by microarray analysis of commensal bacteria-induced immunological changes.
No sample metadata fields
View SamplesSeries of samples studying effect of knock out Emx2 in urogenital epithelium of mouse embryos at E10.5.
Abnormal epithelial cell polarity and ectopic epidermal growth factor receptor (EGFR) expression induced in Emx2 KO embryonic gonads.
No sample metadata fields
View Samples<Objective> To compare gene expression in labial salivary glands (LSG) of IgG4-related disease (IgG4-RD) with Sjgrens syndrome (SS).
DNA microarray analysis of labial salivary glands in IgG4-related disease: comparison with Sjögren's syndrome.
Sex, Specimen part
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