This SuperSeries is composed of the SubSeries listed below.
Molecular heterogeneity in acute renal allograft rejection identified by DNA microarray profiling.
No sample metadata fields
View Samples-catenin signaling is required for hair follicle development, but it is unknown whether it is sufficient to activate expression of hair follicle genes in embryonic skin. To address this we profiled gene expression in dermis from E15.5 KRT14-Cre Ctnnb1(Ex3)fl/+ embryos carrying an activating mutation in epithelial beta-catenin, and control littermate embryos.
Molecular heterogeneity in acute renal allograft rejection identified by DNA microarray profiling.
No sample metadata fields
View Samples-catenin signaling is required for hair follicle development, but it is unknown whether it is sufficient to activate expression of hair follicle genes in embryonic skin. To address this we profiled gene expression in skin dissected from E14.5 KRT14-Cre Ctnnb1(Ex3)fl/+ embryos carrying an activating mutation in epithelial beta-catenin, and control littermate embryos.
Molecular heterogeneity in acute renal allograft rejection identified by DNA microarray profiling.
No sample metadata fields
View Samples-catenin signaling is required for hair follicle development, but it is unknown whether it is sufficient to activate expression of hair follicle genes in embryonic skin. To address this we profiled gene expression in epidermis from E15.5 KRT14-Cre Ctnnb1(Ex3)fl/+ embryos carrying an activating mutation in epithelial beta-catenin, and control littermate embryos.
Molecular heterogeneity in acute renal allograft rejection identified by DNA microarray profiling.
No sample metadata fields
View SamplesThe biopsy samples obtained at implantation segregated in 2 distinct groups according to donor origin, with a cluster of 319 unique identified genes higher expressed in DD compared to LD kidneys, and 329 genes lower expressed (false discovery rate <5%). Using pathway analysis software a significant local renal overrepresentation of complement genes in DD implantation biopsies was identified. Complement gene expression in DD kidneys related both to donor death and cold ischemia duration, and was associated with a slower onset of renal allograft function. In post-transplantation protocol biopsies, there was a continued overexpression of complement genes, regardless of donor source. The local renal complement gene expression variability in post-transplantation biopsies correlated with renal graft function.
Expression of complement components differs between kidney allografts from living and deceased donors.
No sample metadata fields
View SamplesTime course analysis of c-Jun expression at 24h resulted in upregulation of a number of well-known fibrogenesis-associated factors.
Unifying mechanism for different fibrotic diseases.
Specimen part
View SamplesMales are 50% more likely to develop end stage kidney failure compared to women. In this study we wanted to find out the molecular mechanism responsible for this increased risk. We collected kidney samples from patients with and without kidney disease and performed a comprehensive gene expression analysis in healthy and diseased male and female kidneys.
Human and murine kidneys show gender- and species-specific gene expression differences in response to injury.
No sample metadata fields
View SamplesMales are 50% more likely to develop end stage kidney failure compared to women. As a model of the human condition we analyzed gene expression changes in healthy and diseased mouse kidneys.
Human and murine kidneys show gender- and species-specific gene expression differences in response to injury.
No sample metadata fields
View SamplesNuclear export of mRNA is an essential process for eukaryotic gene expression. TREX complex couples the gene expression from transcription and splicing to mRNA export. Sub2, a core component of TREX complex in yeast is diversified to two closely related RNA helicases, UAP56 and URH49 in human.UAP56 and URH49 are required for bulk poly (A)+ RNA export but their target genes are quite different. In conclusion, UAP56 and URH49 have a different function in vivo despite the highly similarity.
The closely related RNA helicases, UAP56 and URH49, preferentially form distinct mRNA export machineries and coordinately regulate mitotic progression.
Cell line
View SamplesMore effective therapeutic approaches for castration-resistant prostate cancer (CRPC) are urgently needed, thus reinforcing the need to understand how prostate tumors progress to castration resistance. We have established a novel mouse xenograft model of prostate cancer, KUCaP-2, which expresses the wild-type androgen receptor (AR) and which produces the prostate-specific antigen (PSA). In this model, tumors regress soon after castration, but then reproducibly restore their ability to proliferate after 1 to 2 months without AR mutation, mimicking the clinical behavior of CRPC. In the present study, we used this model to identify novel therapeutic targets for CRPC. Evaluating tumor tissues at various stages by gene expression profiling, we discovered that the prostaglandin E receptor EP4 subtype (EP4) was significantly upregulated during progression to castration resistance. Immunohistochemical results of human prostate cancer tissues confirmed that EP4 expression was higher in CRPC compared with hormone-nave prostate cancer. Ectopic overexpression of EP4 in LNCaP cells (LNCaP-EP4 cells) drove proliferation and PSA production in the absence of androgen supplementation in vitro and in vivo. Androgen-independent proliferation of LNCaP-EP4 cells was suppressed when AR expression was attenuated by RNA interference. Treatment of LNCaP-EP4 cells with a specific EP4 antagonist, ONO-AE3-208, decreased intracellular cyclic AMP levels, suppressed PSA production in vitro, and inhibited castration-resistant growth of LNCaP-EP4 or KUCaP-2 tumors in vivo. Our findings reveal that EP4 overexpression, via AR activation, supports an important mechanism for castration-resistant progression of prostate cancer. Furthermore, they prompt further evaluation of EP4 antagonists as a novel therapeutic modality to treat CRPC.
Identification of EP4 as a potential target for the treatment of castration-resistant prostate cancer using a novel xenograft model.
Specimen part
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