Induction of dnFGFR2bfor 3 partially overlapping intervals at the early stages of otocyst morphogenesis revealed expected and novel up and downregulated genes that were validated by in situ hybridization analysis. Cell cyle genes were enriched in the downregulated datasets and human hearingloss genes were enriched in the upregulated datasets. Overall design: Differential mRNA expression analysis of pooled Rosa26rtTA/+ (control) and pooled Rosa26rtTA/+;Tg(tetO-s(dn)Fgfr2b)/+ (experimental) embryos induced with doxycycline for the indicated intervals. N=4 biological replicates per treatment (i.e. 4 pregnant females)
Spatial and temporal inhibition of FGFR2b ligands reveals continuous requirements and novel targets in mouse inner ear morphogenesis.
Subject
View SamplesPediatric GIST commonly harbors a disabled succinate dehydrogenase complex (SDH), which yields tumors with highly conserved genomes but characteristic epigenomic signatures. Mysteriously, nearly half of such SDH-deficient GIST, including tumors from Carney Triad patients, lack identifiable mutations in SDH component genes and genes required for complex assembly (SDHA, SDHB, SDHC, SDHD, SDHAF, termed SDHx). Genomic sequencing coupled with DNA methylation and transcriptional profiling have exposed SDHC promoter-specific CpG island epimutation and concomitant gene silencing in the majority of SDHx-WT GIST.
Recurrent epimutation of SDHC in gastrointestinal stromal tumors.
No sample metadata fields
View SamplesWe report specific changes in schizophrenia developmental interneurons by genome-wide transcriptome analysis. Overall design: RNA sequencing analysis (bulk) of healthy control interneurons vs. schizophrenia interneurons. Fourteen independent iPSC lines per group with two independent differentiations
Dysregulated protocadherin-pathway activity as an intrinsic defect in induced pluripotent stem cell-derived cortical interneurons from subjects with schizophrenia.
Specimen part, Disease, Subject
View SamplesWe report down-regulation of protocadeherins in schizophrenia interneurons by genome-wide transcriptome analysis. Overall design: RNA sequencing analysis (bulk) of healthy control interneurons vs. schizophrenia interneurons. Four independent iPS lines per group (total 8 iPSC lines) with three independent differentiations
Dysregulated protocadherin-pathway activity as an intrinsic defect in induced pluripotent stem cell-derived cortical interneurons from subjects with schizophrenia.
Specimen part, Disease, Subject
View SamplesLong chain fatty acids (LCFA) serve as energy sources, components of cell membranes, and precursors for signalling molecules. Here we show that these important biological compounds also regulate gene expression by controlling the transcriptional activities of the retinoic acid (RA)-activated nuclear receptors RAR and PPAR/. Our data indicates that these activities of LCFA are mediated by FABP5, a protein that delivers ligands from the cytosol to nuclear PPAR/. Both saturated and unsaturated LCFA (SLCFA, ULCFA) tightly bind to FABP5, thereby displacing RA and diverting it to RAR. However, while SLCFA inhibit, ULCFA activate the FABP5/PPAR/ pathway. By concomitantly promoting the activation of RAR and inhibiting the activity of PPAR/, SLCFA suppress the growth and oncogenic properties of FABP5-expressing carcinoma cells both in cultured cells and in vivo.
Saturated fatty acids regulate retinoic acid signalling and suppress tumorigenesis by targeting fatty acid-binding protein 5.
Cell line
View SamplesCRABP2 potently suppresses carcinoma cell growth, yet the mechanism(s) that underlie this activity remain incompletely understood. Two distinct functions are known for CRABP2: 1) the classical function of this protein is to directly deliver retinoic acid (RA) to the nuclear retinoic-acid receptorthereby activate gene expression, and 2) in the absence of RA, CRABP2 directly binds to the RNA-binding and stabilizing protein, HuR, and markedly strengthens its interactions with target mRNAs.
Cellular retinoic acid-binding protein 2 inhibits tumor growth by two distinct mechanisms.
Specimen part, Cell line
View SamplesIn order to understand the underlying mechanisms, which ensure that disease progression is prevented in EC, a comprehensive analysis of clinical phenotypes coupled to genetics and biomolecular mechanisms is required. The rapidly increasing accessibility of genetic and biomolecular expression data from new high-throughput technologies is the foundation to shift the traditional phenotype-first approach to explorative genetic or molecular data-first approaches. In this study, we aimed to explore a comprehensive analysis of host transcriptomics and proteomics data coupled to clinical phenotypes in a well-defined Swedish EC cohort with up to 20 years of clinical follow-up data.
Transcriptomics and Targeted Proteomics Analysis to Gain Insights Into the Immune-control Mechanisms of HIV-1 Infected Elite Controllers.
Sex, Age, Specimen part, Disease, Treatment, Race
View SamplesOBJECTIVE: To understand the molecular pathways underlying the cardiac preconditioning effect of short-term caloric restriction (CR). BACKGROUND: Lifelong CR has been suggested to reduce the incidence of cardiovascular disease through a variety of mechanisms. However, prolonged adherence to a CR life-style is difficult. Here we show how short-term CR protects the mouse heart from ischemia. METHODS: Male 10-12 wk old C57bl/6 mice were randomly assigned to an ad libitum (AL) diet with free access to regular chow, or CR, receiving 30% less food over a period of 7 days (d), prior to myocardial infarction (MI) via permanent coronary ligation. Prior to MI (d8), the left ventricles (LV) of AL and CR mice were collected for Western blot, DNA and microRNA (miR) analyses. In separate groups, infarct size, cardiac hemodynamics and protein abundance of caspase 3 was measured at d2 post-MI. RESULTS: This short-term model of CR was associated with cardio-protection, as evidenced by decreased infarct size (18.52.4% vs. 26.61.7%, N=10/group; P=0.01). cDNA and miR profiles pre-MI (N=5/group) identified genes modulated by short-term CR to be associated with circadian clock, oxidative stress, immune function, apoptosis, metabolism, angiogenesis, cytoskeleton and extracellular matrix (ECM). Western blots pre-MI revealed CR-associated increases in phosphorylated Akt and GSK3, reduced levels of phosphorylated AMPK and mitochondrial related proteins PGC-1, cytochrome C and cyclooxygenase (COX) IV, with no differences in the levels of phosphorylated eNOS or MAPK (ERK1/2; p38). CONCLUSIONS: Short-term CR for only 7d represents a preconditioning strategy that limits infarct size. It is associated with a unique gene and miR signature, including the activation of specific pro-survival kinases. These findings may have implications for therapeutic use of short-term CR. .
Cardioprotective Signature of Short-Term Caloric Restriction.
Sex, Specimen part
View SamplesCategorisation of LGGs related to their lesion site (infratentorial vs. supratentorial)
Molecular fingerprinting reflects different histotypes and brain region in low grade gliomas.
No sample metadata fields
View SamplesA single replicate of exponentially growing DT40 CL18 chicken B lymphoma cells were harvested and extracted RNA was subjected to Illumina GAIIx paired-end sequencing to determine global gene expression. Overall design: Single replicate RNA-seq expression analysis of DT40 cells.
Third Report on Chicken Genes and Chromosomes 2015.
Specimen part, Cell line, Subject
View Samples