In this study, we studied the genomic responses of the Insig and Scap deletion from perinatal lung.
Epithelial SCAP/INSIG/SREBP signaling regulates multiple biological processes during perinatal lung maturation.
Specimen part
View SamplesBackground: Lung function is dependent upon the precise regulation of the synthesis, storage, and catabolism of tissue and alveolar lipids.
Activation of sterol-response element-binding proteins (SREBP) in alveolar type II cells enhances lipogenesis causing pulmonary lipotoxicity.
Specimen part
View SamplesIn this study, time dependent genome wide lung mRNA profiling changes were assessed using C57BL/6J and A/J mice. Through comprehensive bioinformatics and functional genomics analyses, we identified both temporal and strain dependent gene expression patterns, systemically mapped key regulators, bioprocesses, and transcriptional networks controlling lung maturation, providing the basis for new therapeutic strategies to enhance lung function in preterm infants.
Transcriptional programs controlling perinatal lung maturation.
Specimen part, Time
View SamplesProliferative and replicative senescent fibroblasts from aged human donors were reprogrammed towards pluripotency and re-differentiated in fibroblasts and then further analyzed for rejuvenation assessment.
Rejuvenating senescent and centenarian human cells by reprogramming through the pluripotent state.
Specimen part, Cell line
View Samplescomparative expression between stromal MS5 cells treated with (MS5_PD18) or without (MS5_DMSO) MEKi
Interleukin-18 produced by bone marrow-derived stromal cells supports T-cell acute leukaemia progression.
Cell line
View SamplesAnalysis of GPR120 which play roles for the fatty acid sensor in adipose tissue. Results provide insight into the transcriptional effects caused by the loss of the GPR120 proteins and provide further insight into their functions.
Dysfunction of lipid sensor GPR120 leads to obesity in both mouse and human.
Specimen part, Treatment, Subject
View SamplesTo understand the the effect of antagomir-17 treatment on human endothelial cells derived from human umbilical cord blood (UCB) CD34+ hematopoietic stem cells, we have employed mRNA sequencing. The antagomiR-17 used in this study was purchased from Dharmacon and cell transfection was performed using Lipofectamine RNAiMAx from Life Technologies. Scramble antagomiR from Ambion was used as control. Cells were transfected with antagomiR-17 or scrambled antagomiR for 48 hours. After 48 h, the cells were collected, RNA was isolated and RNA samples were shipped to Exiqon Services, Denmark for mRNA sequencing. All sequencing experiments (RNA integrity measurements, library preparation and next generation sequencing) were conducted at Exiqon Services, Denmark. Overall design: CD34+ endothelial cells differentiated from umbilical cord blood hematopoietic stem cells (CD34+) were treated with 50 nM antagomiR-17 (Dharmacon) or scrambled antagomiR (Ambion) using Lipofectamine RNAiMAx (Life Technologies) for 48 h. Three replicates were used for each condition (i.e. antagomiR-17 and scramble antagomiR conditions).
Synthetic microparticles conjugated with VEGF<sub>165</sub> improve the survival of endothelial progenitor cells via microRNA-17 inhibition.
No sample metadata fields
View SamplesThe FBXL10 protein (also known as KDM2B, JHDM1B, CXXC2, and NDY1) is bound to essentially all CpG-rich promoters in the mammalian genome. FBXL10 is expressed as two isoforms: FBXL10-1, a longer form that contains an N-terminal JmjC domain with C- terminal F-box, CXXC, PHD, RING, and leucine rich repeat (LRR) domains, and FBXL10-2, a shorter form that initiates at an alternative internal exon and which lacks the JmjC domain but retains the other domains. Selective deletion of Fbxl10-1 had been reported to produce a minor and variable phenotype, and most mutant animals were essentially normal. We show here that deletion of Fbxl10-2 (in a manner that does not perturb expression of Fbxl10-1) resulted in a very different phenotype with craniofacial abnormalities, greatly increased lethality, and female sterility in surviving homozygous mutants. The phenotype of the Fbxl10-2 deletion was more severe in female mutants. We found that mutants that lacked both FBXL10-1 and -2 showed embryonic lethality and even more extreme sexual dimorphism, with more severe gene dysregulation in mutant female embryos. X-linked genes were most severely dysregulated, and there was marked overexpression of Xist in mutant females although genes that encode factors that bind to Xist RNA were globally down-regulated in mutant female as compared to male embryos. FBXL10 is the first factor shown to be required both for the normal expression and function of the Xist gene. Overall design: Expression analysis using RNA-seq was performed on WT and Fbxl10T/T male and female embryos.
Abnormal X chromosome inactivation and sex-specific gene dysregulation after ablation of FBXL10.
Sex, Specimen part, Cell line, Subject
View SamplesEffect of either FLO8 or MSS11 deletion and -overexpression on yeast transcript profiles compared to wild type in laboratory yeast strains 1278b and S288c - also the effect of FLO11 (MUC1) overexpression in the 1278b genetic background
Many Saccharomyces cerevisiae Cell Wall Protein Encoding Genes Are Coregulated by Mss11, but Cellular Adhesion Phenotypes Appear Only Flo Protein Dependent.
No sample metadata fields
View SamplesIn this study, we have investigated the role of secondhand smoke (SHS) in the development of metabolic liver disease by characterizing the global regulation of genes and molecular pathways in SHS-exposed mice after termination of exposure (SHS 4M) and following one-month recovery in clean air (SHS 4M +1M RECOVERY).
Secondhand Smoke Induces Liver Steatosis through Deregulation of Genes Involved in Hepatic Lipid Metabolism.
Sex
View Samples