The discovery of genetic variants in the CHRNA5-CHRNA3-CHRNB4 gene cluster associated with heavy smoking and higher relapse risk has led to the identification of the midbrain habenula- interpeduncular axis as a critical relay circuit in the control of nicotine addiction
Reexposure to nicotine during withdrawal increases the pacemaking activity of cholinergic habenular neurons.
Specimen part, Disease
View SamplesThe integration of the results of QTL fine-mapping with microarray expression data offers a promising tool for understanding the genetic mechanisms influencing complex traits as fatty acid composition in pigs. The expression level of each probe may be treated as a quantitative trait and the marker genotypes used to map loci with regulatory effect on the gene expression level (eQTL)
Genome-wide analysis of porcine backfat and intramuscular fat fatty acid composition using high-density genotyping and expression data.
Sex, Age
View SamplesIdentification of genes and causal mutations regulating growth and fatness traits in pig. Overall design: Transcriptome sequencing of 10 liver samples of two groups of divergent pigs for growth and fatness.
Using RNA-Seq SNP data to reveal potential causal mutations related to pig production traits and RNA editing.
Sex, Age, Specimen part, Subject
View SamplesReactive oxygen species (ROS) are implicated in tumor transformation by modulating proteins involved in differentiation, proliferation and invasion. In order to identify genes that may support melanoma progression or regression after an antioxidant system (AOS) response, we developed and characterized a human melanoma cell model with different levels of ROS by stably overexpressing the antioxidant enzyme catalase in A375 amelanotic melanoma cells, and whole genome gene expression patterns were analyzed by microarrays.
Reprogramming human A375 amelanotic melanoma cells by catalase overexpression: Upregulation of antioxidant genes correlates with regression of melanoma malignancy and with malignant progression when downregulated.
Specimen part, Cell line
View SamplesThese data represents a microgenomic approach to dissect the response of the plant steroid hormone, brassinosteroid, in the provascular tissue of the arabidopsis thaliana primary roots. We used two different provascular markers, wooden leg (WOL) and corona (ATHB15) to profile the provascular response to BRs. We used a timecourse analysis with 4 different timepoint; 0.5, 1, 2 and 4 hours treated with BRs in the WOL domain. Additional trasncriptomic responses of the ATHB15 domain were analyzed after 2 hours BRs treatment.
Regulation of plant stem cell quiescence by a brassinosteroid signaling module.
Specimen part, Time
View SamplesMice selected for high and low acute inflammation were tested for pristane induced arthritis, showing to be susceptible and resistant, respectively.
Pristane-induced arthritis loci interact with the Slc11a1 gene to determine susceptibility in mice selected for high inflammation.
Sex, Age, Specimen part
View SamplesDUSP1 is involved in different cellular pathways including cancer cell proliferation, angiogenesis, invasion and resistance to chemotherapy. To understand more about the cellular responses regulated by DUSP1 in NSCLC cells, we interfered DUSP1 expression in the NSCLC cell line H460 and studied the changes in gene expression differentially regulated by this phosphatase.
DUSP1/MKP1 promotes angiogenesis, invasion and metastasis in non-small-cell lung cancer.
Specimen part, Cell line
View SamplesLeft ventricular noncompaction (LVNC) Causes prominent ventricular trabeculations and reduces cardiac systolic function. The clinical presentation of LVNC ranges from asymptomatic to heart failure. We show that germline mutations in human MIB1 (mindbomb homolog 1), which encodes an E3 ubiquitin ligase that promotes endocytosis of the NOTCH ligands DELTA and JAGGED, cause LVNC in autosomal-dominant pedigrees, with affected individuals showing reduced NOTCH1 activity and reduced expression of target genes. Functional studies in cells and zebrafish embryos and in silico modeling indicate that MIB1 functions as a dimer, which is disrupted by the human mutations. Targeted inactivation of Mib1 in mouse myocardium causes LVNC, a phenotype mimicked by inactivation of myocardial Jagged1 or endocardial Notch1. Myocardial Mib1 mutants show reduced ventricular Notch1 activity, expansion of compact myocardium to proliferative, immature trabeculae and abnormal expression of cardiac development and disease genes. These results implicate NOTCH signaling in LVNC and indicate that MIB1 mutations arrest chamber myocardium development, preventing trabecular maturation and compaction. Overall design: RNA was isolated from the ventricles of 16 WT and 16 Mib1flox; CTnT-cre hearts at E14.5 and then pooled into four replicates.
Mutations in the NOTCH pathway regulator MIB1 cause left ventricular noncompaction cardiomyopathy.
No sample metadata fields
View SamplesToca 511 is a modified Retroviral Replicating Vector based on Moloney g-retrovirus with an amphotropic envelope. As an investigational cancer treatment, Toca 511 preferentially infects cancer cells without direct cell lysis and encodes an enhanced yeast cytosine deaminase that converts the antifungal drug 5-fluorocytosine to the anticancer drug, 5-fluorouracil. A panel of established human cancers cell lines, derived from glioblastoma, colon, and breast cancer tissue was used to evaluate parameters critical for effective anticancer activity. As part of these analyses, we profiled relative mRNA levels across these cell lines via RNA sequencing. Overall design: mRNA expression profiles across nine human cancer cell lines.
Retroviral Replicating Vectors Deliver Cytosine Deaminase Leading to Targeted 5-Fluorouracil-Mediated Cytotoxicity in Multiple Human Cancer Types.
No sample metadata fields
View SamplesAIRmax and AIRmin mouse lines show a differential lung inflammatory response and differential lung tumor susceptibility after urethane treatment, thus constituting a good genetic model to investigate differences in gene expression profiles related to inflammatory response and lung tumor susceptibility. The transcript profile of ~24,000 known genes was analyzed in normal lung tissue of untreated and urethane-treated AIRmax and AIRmin mice. In lungs of untreated mice, inflammation associated genes involved in pathways such as leukocyte transendothelial migration, cell adhesion and tight junctions were differentially expressed in AIRmax versus AIRmin mice. Moreover, gene expression levels differed significantly in urethane-treated mice even at 21 days after treatment. In AIRmin mice, modulation of expression of genes involved in pathways associated with inflammatory response paralleled the previously observed persistent infiltration of inflammatory cells in the lung of these mice. In conclusion, a specific gene expression profile in normal lung tissue is associated with mouse line susceptibility or resistance to lung tumorigenesis and with different inflammatory response, and urethane treatment causes a long-lasting alteration of the lung gene expression profile that correlates with persistent inflammatory response of AIRmin mice.
Transcriptome of normal lung distinguishes mouse lines with different susceptibility to inflammation and to lung tumorigenesis.
Sex, Specimen part
View Samples