Genome-wide alternative splice analysis of RNA from lupus and its severe form lupus nephritis
Genome-wide peripheral blood transcriptome analysis of Arab female lupus and lupus nephritis.
Sex, Specimen part, Disease stage
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Mutations in the RNA granule component TDRD7 cause cataract and glaucoma.
Specimen part, Cell line
View SamplesAnalysis of Tdrd7 deficiency in mouse lens epithelial-derived cell line at gene expression level. The hypothesis tested was that Tdrd7 is involved in post-transcriptional control of gene expression in the lens. Results provide evidence for differential regulation of genes involved in lens homeostasis and cataract formation in the absence of Tdrd7.
Mutations in the RNA granule component TDRD7 cause cataract and glaucoma.
Specimen part, Cell line
View SamplesAnalysis of Tdrd7 deficiency in mouse lens epithelial-derived cell line at gene expression level. The hypothesis tested was that Tdrd7 is involved in post-transcriptional control of gene expression in the lens. Results provide evidence for differential regulation of genes involved in lens homeostasis and cataract formation in the absence of Tdrd7.
Mutations in the RNA granule component TDRD7 cause cataract and glaucoma.
Specimen part
View SamplesAnalysis of Tdrd7 deficiency in mouse lens epithelial-derived cell line at gene expression level. The hypothesis tested was that Tdrd7 is involved in post-transcriptional control of gene expression in the lens. Results provide evidence for differential regulation of genes involved in lens homeostasis and cataract formation in the absence of Tdrd7.
Mutations in the RNA granule component TDRD7 cause cataract and glaucoma.
Specimen part
View SamplesEnzalutamide (formerly MDV3100 and available commercially as Xtandi), a novel androgen receptor (AR) signaling inhibitor, blocks the growth of castration-resistant prostate cancer (CRPC) in cellular model systems and was shown in a clinical study to increase survival in patients with metastatic CRPC. Enzalutamide inhibits multiple steps of AR signaling: (1) binding of androgens to AR, (2) AR nuclear translocation, and (3) association of AR with DNA.
Enzalutamide, an androgen receptor signaling inhibitor, induces tumor regression in a mouse model of castration-resistant prostate cancer.
Specimen part, Cell line
View SamplesADAMs are transmembrane metalloproteases that control cell behavior by cleaving both cell adhesion and signaling molecules. The cytoplasmic domain of ADAMs can regulate the proteolytic activity by controlling the subcellular localization and/or the activation of the protease domain. Here we show that the cytoplasmic domain of ADAM13 is cleaved and translocates into the nucleus. Preventing this translocation renders the protein incapable of promoting cranial neural crest (CNC) cell migration in vivo, without affecting its proteolytic activity. In addition, the cytoplasmic domain of ADAM13 regulates the expression of multiple genes in the CNC. This study shows that the cytoplasmic domain of ADAM metalloproteases can perform essential functions in the nucleus of cells and may contribute substantially to the overall function of the protein.
Translocation of the cytoplasmic domain of ADAM13 to the nucleus is essential for Calpain8-a expression and cranial neural crest cell migration.
Specimen part
View SamplesWe aim to identify genes differentially expressed between mouse WT and COUP-TFI_Nex-Cre mutant cortices.
Postmitotic control of sensory area specification during neocortical development.
Specimen part
View SamplesThe goal of the microarray experiment was to identify genes that were differentially expressed in NAD-treated and water-treated sweet orange leaf tissues. Results indicated that, compared with the water treatment, the NAD tretament triggered profound transcriptome changes in the citrus leaves, with about 1,200 genes being up-regulated or down-regulated by twofold or more.
Exogenous Nicotinamide Adenine Dinucleotide Induces Resistance to Citrus Canker in Citrus.
Specimen part, Time
View SamplesCellular identity is determined by its gene expression programs. The ability of the cell to change its identity and produce cell types outside its lineage is achieved by the activity of transcription controllers capable of reprogramming differentiation gene networks. The synovial sarcoma associated protein, SYT-SSX2, reprograms myogenic progenitors and human bone marrow-derived mesenchymal stem cells (BMMSCs) by dictating their commitment to a pro-neural lineage. It fulfills this function by directly targeting an extensive array of neural-specific genes as well as genes of developmental pathway mediators. Concomitantly, the ability of both myoblasts and BMMSCs to differentiate into their normal myogenic and adipogenic lineages was compromised. Synovial sarcoma is believed to arise in mesenchymal stem cells where formation of the t(X;18) translocation product, SYT-SSX, constitutes the primary event in the cancer. SYT-SSX is therefore believed to initiate tumorigenesis in its target stem cell. The data presented here allow a glimpse at the initial events that likely occur when SYT-SSX2 is first expressed and its dominant function in subverting the nuclear program of the stem cell, leading to its aberrant differentiation, as a first step toward transformation. In addition, we identified the fibroblast growth factor receptor gene, Fgfr2, as one occupied and upregulated by SYT-SSX2. Knockdown of FGFR2 in both BMMSCs and synovial sarcoma cells abrogated their growth and attenuated their neural phenotype. These results support the notion that the SYT-SSX2 nuclear function and differentiation effects are conserved throughout sarcoma development and are required for its maintenance beyond the initial phase. They also provide the stem cell regulator, FGFR2 as a promising candidate target for future synovial sarcoma therapy.
Reprogramming of mesenchymal stem cells by the synovial sarcoma-associated oncogene SYT-SSX2.
Specimen part
View Samples