Summary:
HCaRG increases renal cell migration by a TGF-alpha autocrine loop mechanism.
No sample metadata fields
View SamplesHEK293 cells were transfected with control plasmid (pcDNAI/Neo;Invitrogen) or with the plasmid encoding HCaRG. Stable transfectants were synchronized and grown in the presence of 10% FBS for 48 h. Total RNAs were purified with the mini RNeasy kit (Qiagen).
HCaRG increases renal cell migration by a TGF-alpha autocrine loop mechanism.
No sample metadata fields
View SamplesDespite timely and successful surgery, 32% of patients with bilateral and 10% with unilateral cryptorchidism will develop azoospermia. Cryptorchid boys at risk of azoospermia display a typical testicular histology of impaired mini-puberty at the time of the orchidopexy.
Testicular gene expression in cryptorchid boys at risk of azoospermia.
Specimen part
View SamplesThe aim of the experiment is to determine sugar and ABA responsive gene expression in Arabidopsis.
Establishing glucose- and ABA-regulated transcription networks in Arabidopsis by microarray analysis and promoter classification using a Relevance Vector Machine.
Age, Time
View SamplesDetermination of the mechanism by which microglia regulate growth of brain tumor initiating cells (BTICs) and differentiation. Results identify the factors involved in the regulation and provide mechanistic basis.
Therapeutic activation of macrophages and microglia to suppress brain tumor-initiating cells.
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.
Age, Specimen part, Cell line, Treatment
View SamplesAmplification of the MYCN oncogene predicts treatment resistance in childhood neuroblastoma. Using a MYC target gene signature that predicts poor neuroblastoma prognosis we identified the histone chaperone, FAcilitates Chromatin Transcription (FACT), as a crucial mediator of the MYC signal and a therapeutic target in the disease. FACT and MYCN expression created a forward feedback loop in neuroblastoma cells that was essential for maintaining mutual high expression. FACT inhibition by the small molecule Curaxin compound, CBL0137, markedly reduced tumor initiation and progression in vivo. CBL0137 exhibited strong synergy with chemotherapy in standard use by blocking repair of DNA damage caused by genotoxic drugs, thus creating a synthetic lethal environment in MYCN amplified neuroblastoma cells and a treatment strategy for MYCN-driven neuroblastoma
Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.
Cell line, Treatment
View SamplesAmplification of the MYCN oncogene predicts treatment resistance in childhood neuroblastoma. Using a MYC target gene signature that predicts poor neuroblastoma prognosis we identified the histone chaperone, FAcilitates Chromatin Transcription (FACT), as a crucial mediator of the MYC signal and a therapeutic target in the disease. FACT and MYCN expression created a forward feedback loop in neuroblastoma cells that was essential for maintaining mutual high expression. FACT inhibition by the small molecule Curaxin compound, CBL0137, markedly reduced tumor initiation and progression in vivo. CBL0137 exhibited strong synergy with chemotherapy in standard use by blocking repair of DNA damage caused by genotoxic drugs, thus creating a synthetic lethal environment in MYCN amplified neuroblastoma cells and a treatment strategy for MYCN-driven neuroblastoma
Therapeutic targeting of the MYC signal by inhibition of histone chaperone FACT in neuroblastoma.
Cell line, Treatment
View SamplesThis file contains gene microarray data from subsets of human intestinal dendritic cells, as defined by their expression of CD103 and Sirpa. This will allow for better understanding of human intestinal DC subsets in general and will facilitate translation from findings in the mouse.
Comparative transcriptional and functional profiling defines conserved programs of intestinal DC differentiation in humans and mice.
Specimen part
View SamplesNK cells are believed to contribute to the control of hepatitis C virus infection and pathogenesis of liver disease. Standard treatment of both acute and chronic hepatitis C is based on the administration of interferon alpha, however, the effects of type I interferons on human NK cells have not been studied in the context of hepatitis C. We therefore first performed a microarray screen for genes differentially regulated in human NK cells after stimulation of PBMC with recombinant interferon alpha-2b. One of the genes upregulated was TRAIL which was confirmed in vitro on the protein level.
Interferon-alpha-induced TRAIL on natural killer cells is associated with control of hepatitis C virus infection.
Sex, Specimen part, Treatment
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