In order to define the transcriptional network functionally regulated by Pax8 as well as infer its direct targets, we performed RNAi to knock-down Pax8 gene in FRTL-5 thyroid cells. Expression data from three independent silencing experiments were analyzed by microarray technology unraveling 2815 genes differentially expressed between silenced cells and controls. Of these, 1421 genes were down-regulated and 1394 genes were up-regulated 72hrs after Pax8 silencing.
Identification of novel Pax8 targets in FRTL-5 thyroid cells by gene silencing and expression microarray analysis.
Cell line
View SamplesPlants are known to be responsive to volatiles, but knowledge about the molecular players involved in transducing their perception remain scarce.
WRKY40 and WRKY6 act downstream of the green leaf volatile E-2-hexenal in Arabidopsis.
Treatment
View SamplesAmyotrophic lateral sclerosis (ALS) is a fatal adult-onset neuromuscular disorder characterized by the selective degeneration of upper and lower motor neurons, progressive muscle wasting and paralysis. To define the full set of alterations in gene expression in skeletal muscle during the course of the disease, we performed high-density oligonucleotide microarray analysis of gene expression in hind limb skeletal muscles of sod1(G86R) mice, one of the existing transgenic models of ALS. To monitor denervation-dependent gene expression, we determined the effects of short-term acute denervation on the muscle transcriptome after sciatic nerve axotomy.
Gene profiling of skeletal muscle in an amyotrophic lateral sclerosis mouse model.
Sex, Age, Specimen part, Disease, Disease stage, Treatment, Subject, Time
View SamplesThe equilibrium between cellular differentiation and proliferation is fundamental for tissue homeostasis. This is particularly important for the liver, a highly differentiated organ with systemic metabolic functions still endowed with unparalleled regenerative potential. Hepatocellular de-differentiation and uncontrolled proliferation are at the basis of liver carcinogenesis. We have identified SLU7, a pre-mRNA splicing regulator inhibited in hepatocarcinoma as a pivotal gene for hepatocellular homeostasis. SLU7 knockdown in human liver cells and mouse liver resulted in profound changes in pre-mRNA splicing and gene expression, leading to impaired glucose and lipid metabolism, refractoriness to key metabolic hormones, and reversion to a fetal-like gene expression pattern. Hepatocellular proliferation and a switch to a tumor-like glycolytic phenotype were also observed. Mechanistically, SLU7 governed the splicing and/or expression of essential genes for hepatocellular differentiation like SRSF3 and HNF4a, and was identified as a critical factor in cAMP-regulated gene transcription. SLU7 is therefore central for hepatocyte identity and quiescence.
Splicing regulator SLU7 is essential for maintaining liver homeostasis.
Cell line
View SamplesCharacterize the gpm1 mutant growth on dual substrate of ethanol and glycerol
Phosphoglycerate mutase knock-out mutant Saccharomyces cerevisiae: physiological investigation and transcriptome analysis.
No sample metadata fields
View SamplesWe have studied the genes activated in human liver transplantation to identify potential target genes for the prevention or treatment of related injuries.
Wide gene expression profiling of ischemia-reperfusion injury in human liver transplantation.
Sex, Age, Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Identification of key regions and genes important in the pathogenesis of sezary syndrome by combining genomic and expression microarrays.
Specimen part, Disease
View SamplesThis study used tumour and paired normal samples from 28 Szary Syndrome (SS) patients to define recurrent regions of chromosomal aberrations. Our data identified recurrent losses of 17p13.2-p11.2 and 10p12.1-q26.3 occurring in 71 and 68% of cases respectively; common gains were detected for 17p11.2-q25.3 (64%) and chromosome 8/8q (50%). Moreover, we identified novel genomic lesions recurring in more than 30% of tumours: loss of 9q13-q21.33 and gain of 10p15.3-10p12.2. In the Szary Syndrome cases analysed, we could find several small and few large Uniparental Disomies involving interstitial or telomeric regions of LOH occurring mainly for chromosome 10 and to a lesser extent for chromosome 9 and 17. In the attempt to correlate Copy Number data and clinical parameters we find a relationship between complex pattern of chromosomal aberrations, involving at least three recurrent Copy Number alterations, and shorter survival. Integrating mapping and transcriptional data we were able to identify a total of 113 deregulated transcripts in aberrant chromosomal regions that included cancer related genes such as members of the NF-kB pathway (BAG4, BTRC, NKIRAS2, PSMD3, TRAF2) that might explain its constitutive activation in CTCL. Matching this list of genes with those discriminating patients with different survival times we identify several common candidates that might exert critical roles in Szary Syndrome, like BUB3 and PIP5K1B.
Identification of key regions and genes important in the pathogenesis of sezary syndrome by combining genomic and expression microarrays.
Specimen part, Disease
View SamplesLiving organisms have to cope with multiple and combined fluctuations in their environment. According to their sessile mode of life, plants are even more subjected to such fluctuations impacting their physiology and development. In particular, nutrient availability is known to tune plant development through modulating hormonal signaling, and conversely, hormonal signals are key to control nutrient related signaling pathways (Krouk et al., 2011a). However, very few is known about molecular mechanisms leading to plant adaptation to such combined signals. Here we deployed an unprecedented combinatorial treatment matrix to reveal plant adaptation in response to nitrate (NO3-), ammonium (NH4+), auxin (IAA), cytokinins (CK) and abscisic acid (ABA) and their exhaustive binary combinations.
Combinatorial interaction network of transcriptomic and phenotypic responses to nitrogen and hormones in the Arabidopsis thaliana root.
Specimen part, Time
View SamplesHER2 is a tyrosine kinase receptor causally involved in cancer. A subgroup of breast cancer patients with particularly poor clinical outcome expresses a heterogeneous collection of HER2 carboxy-terminal fragments (CTFs). However, since the CTFs lack the extracellular domain that drives dimerization and subsequent activation of full-length HER2, they are in principle expected to be inactive. Here we present evidence that at low expression levels one of these fragments, 611-CTF, activated multiple signaling pathways because of its unanticipated ability to constitutively homodimerize. A transcriptomic analysis revealed that 611-CTF specifically controlled the expression of genes that we found correlated with poor prognosis in breast cancer. Among the 611-CTF-regulated genes were several that previously have been linked to metastasis, including MET, EPHA2, MMP1, IL11, ANGPTL4 and different Integrins. Transgenic mice overexpressing HER2 in the mammary gland develop tumors only after acquisition of activating mutations in the transgene. In contrast, we show that expression of 611-CTF led to development of aggressive and invasive mammary tumors without the need for mutations. These results demonstrate that 611-CTF is a potent oncogene capable of promoting mammary tumor progression and metastasis.
A naturally occurring HER2 carboxy-terminal fragment promotes mammary tumor growth and metastasis.
Cell line, Time
View Samples