Project description:Comparison of the gene expression profiles between normal and Fgfrl1 deficient kidneys 3 individual RNA preparations from 6-9 pooled normal kidneys each vs. 3 individual RNA preparations from 6-9 Fgfrl1-/- kidneys each
Project description:Several genes were indicated as genes strongly affected by FGFRL1-deficiency, through expression profiling of a total of 25,000 genes in 2 wild type KYSE520 human oesphageal squamous cell carcinoma cells and 2 FGFRL1-deficient kYSE520 cells
Project description:FGFRs regulate PCa development and progression, but the role of the recently found FGFR-like 1 (FGFRL1, FGFR5) remains unclear. The data consists of gene expression profiles of FGF13 and FGFRL1 knock-down PC3M prostate cancer cells compared to control cells.
Project description:FGFRs regulate PCa development and progression, but the role of the recently found FGFR-like 1 (FGFRL1) remains unclear. The data consists of gene expression profiles of mouse subcutanous xenograft tumors generated of human PC3M prostate cancer cells with stable knockdown of FGFRL1 gene and of the control xenografts.
Project description:Analysis of ovarian cancer cell lines after knockdown of FGFRL1 using SiRNA. To elucidate the signaling pathways that were significantly altered following the silencing of FGFRL1 expression, we performed global gene profiling experiments of the OVCAR8 and ES2 cells after knockdown of FGFRL1 using siRNA. We conducted pathway analysis with the differentially expressed genes using R in two OC cells.
Project description:Despite 30 years of Hox gene study we have a remarkably limited knowledge of the downstream target genes that Hox transcription factors regulate to confer regional identity. Here, we have used a microarray approach to identify genes that function downstream of a single vertebrate Hox gene, zebrafish hoxb1a. This gene plays a critical and conserved role in vertebrate hindbrain development, conferring identity to hindbrain rhombomere 4. For example, zebrafish Hoxb1a, similar to mouse Hoxb1, is required for the migration of r4-derived facial branchiomotor neurons into the posterior hindbrain. We have screened microarrays carrying more than 16,000 expressed sequence tags (ESTs) for genes that are differentially regulated in normal versus Hoxb1a-deficient rhombomere 4 tissue. Using this approach, we have identified both positively and negatively regulated candidate Hoxb1a target genes. We have used in situ hybridization to validate twelve positively regulated Hoxb1a targets. These downstream targets are expressed in a variety of subdomains within r4, with one gene, a novel prickle homolog (pk1b), expressed specifically within the facial branchiomotor neurons. Using morpholino knock-down we show that the Hoxb1a target Pk1b is required for facial neuron migration, a single aspect of rhombomere 4 identity. Keywords: Comparison of normal and Hox-deficient tissue
Project description:Notch signaling deficient kidney collecting ducts may serve as a useful resource to identify principal cell lineage and intercalated lineage specific factors since they develop a reduced number of principal cells and an increased number of intercalated cells compared with wild type kidney collecting ducts. We compared RNA from three E18.5 mouse kidneys per group: HoxB7Cre;RBPJf/-;Rosa+/Eyfp (Notch signaling deficient; mutant) versus RBPJf/f;Rosa+/Eyfp (wild type).
Project description:Methylation array analyses of 30 CCSKs in comparison with 18 Wilms tumours and normal non-malignant kidneys (2 foetal kidneys and 6 adult kidneys) revealed CCSK tumour DNA to be globally hypermethylated. Four CCSKs, two WTs, two foetal kidneys and 2 adult kidneys were analysed as technical duplicates on different arrays.
Project description:Malignant peripheral nerve sheath tumor (MPNST) is a type of soft tissue sarcoma that occurs in carriers of mutations in the neurofibromatosis type I gene (Nf1) as well as sporadically. Plexiform neurofibromas in NF1 patients have a significant risk of developing into MPNSTs leading to increased morbidity and mortality from this syndrome. Surgery is the primary intervention but it is not always effective due to the tendency of MPNSTs to infiltrate the surrounding tissue or grow in an inoperable location. Neurofibromin, the protein coded by the Nf1 gene, functions as a GTPase activating protein (GAP) whose mutation leads to constitutive activation of RAS and mitogen-activated protein kinase (MAPK) signaling in NF1 patients’ tumors. However, therapeutic targeting of RAS and MAPK have had limited success (Kalamarides, et al., 2012). In this study, we modulated NRAS, MEK1/2 and neurofibromin levels in MPNST cell lines and determined the global gene expression changes that were associated with each experimental condition. Furthermore, gene expression changes due to neurofibromin deficiency but independent of NRAS and MEK1/2 regulation were characterized for the first time in MPNST cell lines. There are total 4 comparison scenarios. Each scenario has two different samples to compare and each sample has three replicates. Comparison 1: ST88-14 cell line versus normal human schwann cell; comparison 2: U0126 treated ST88-14 versus DMSO treat ST88-14 as control; comparison 3: siNRAS treated ST88-14 versus scrambled control treated ST88-14 cell line; comparison 4: siNf1 treated STS26T cell line versus scrambled control RNA treated STS26T cell line.