Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA276638 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:LB-22 is an immortalized mesenchymal cell line derived from embryonic kidneys of 'immortomice'. Immortomice ubiquitously express an interferon-inducible, temperature-sensitive SV-40 large T antigen. LB-22 cells were selected for endogenous abundant expression of the mouse Wilms' tumor suppressor homolog WT1, an important transcription factor in kidney development. Here, we assessed changes in gene expression in response to siRNA mediated WT1 knockdown.
2015-02-28 | GSE66356 | GEO
Project description:LB-22 is an immortalized mesenchymal cell line derived from embryonic kidneys of 'immortomice'. Immortomice ubiquitously express an interferon-inducible, temperature-sensitive SV-40 large T antigen. LB-22 cells were selected for endogenous abundant expression of the mouse Wilms' tumor suppressor homolog WT1, an important transcription factor in kidney development. Here, we assessed changes in gene expression in response to siRNA mediated WT1 knockdown. LB-22 cells were transfected either with WT1 siRNA or scramble Control siRNA. Total RNA was extracted 48 hours after transfection and Affymetrix Mouse 430.2 expression arrays were hybridized according to standard protocols. CEL files not available for this dataset.
2015-02-28 | E-GEOD-66356 | biostudies-arrayexpress
Project description:We report the the identification of chrosomal regions bound by the Wilms' tumor suppressor gene WT1 during embryonic mouse kidney development. Two indepednent ChIP-Seq experiments on microdissected E18.5 developing mouse kidneys were carried out using either WT1-specific or IgG-antibodies as a negative control.
2014-06-15 | E-GEOD-58179 | biostudies-arrayexpress
Project description:RNA sequencing was performed in samples isolated from primary normal airway epithelial cells, primary dysplastic airway epithelial cells (SPORE 43672) and immortalized cells (AALE), all of which were either transfected with control siRNA or with siRNA promoting the knockdown of the transcriptional regulators YAP (YAP1) and TAZ (WWTR1).
2021-06-08 | GSE133003 | GEO
Project description:We report the the identification of chrosomal regions bound by the Wilms' tumor suppressor gene WT1 during embryonic mouse kidney development.
2014-06-15 | GSE58179 | GEO
Project description:The Wilms tumor-suppressor gene WT1, a key player in renal development, also has a crucial role in maintenance of the glomerulus in the mature kidney. However, molecular pathways orchestrated by WT1 in podocytes, where it is highly expressed, remain unknown. Their defects are thought to modify the cross-talk between podocytes and other glomerular cells and ultimately lead to glomerular sclerosis, as observed in diffuse mesangial sclerosis (DMS) a nephropathy associated with WT1 mutations. To identify podocyte WT1 targets, we generated a novel DMS mouse line, performed gene expression profiling in isolated glomeruli, and identified excellent candidates that may modify podocyte differentiation and growth factor signalling in glomeruli. Scel, encoding sciellin, a protein of the cornified envelope in the skin, and sulf1, encoding a 6-O endosulfatase, are shown to be expressed in wild type podocytes and to be strongly down-regulated in mutants. Co-expression of Wt1, Scel and Sulf1 was also found in a mesonephric cell line, and siRNA-mediated knockdown of WT1 decreased Scel and Sulf1 mRNAs and proteins. By ChIP we show that Scel and Sulf1 are direct WT1 targets. Cyp26a1, encoding an enzyme involved in the degradation of retinoic acid, is shown to be up-regulated in mutant podocytes. Cyp26a1 may play a role in the development of glomerular lesions but does not seem to be regulated by WT1. These results provide novel clues in our understanding of normal glomerular function and early events involved in glomerulosclerosis.
2009-10-02 | GSE18358 | GEO
Project description:The Wilms tumor-suppressor gene WT1, a key player in renal development, also has a crucial role in maintenance of the glomerulus in the mature kidney. However, molecular pathways orchestrated by WT1 in podocytes, where it is highly expressed, remain unknown. Their defects are thought to modify the cross-talk between podocytes and other glomerular cells and ultimately lead to glomerular sclerosis, as observed in diffuse mesangial sclerosis (DMS) a nephropathy associated with WT1 mutations. To identify podocyte WT1 targets, we generated a novel DMS mouse line, performed gene expression profiling in isolated glomeruli, and identified excellent candidates that may modify podocyte differentiation and growth factor signalling in glomeruli. Scel, encoding sciellin, a protein of the cornified envelope in the skin, and sulf1, encoding a 6-O endosulfatase, are shown to be expressed in wild type podocytes and to be strongly down-regulated in mutants. Co-expression of Wt1, Scel and Sulf1 was also found in a mesonephric cell line, and siRNA-mediated knockdown of WT1 decreased Scel and Sulf1 mRNAs and proteins. By ChIP we show that Scel and Sulf1 are direct WT1 targets. Cyp26a1, encoding an enzyme involved in the degradation of retinoic acid, is shown to be up-regulated in mutant podocytes. Cyp26a1 may play a role in the development of glomerular lesions but does not seem to be regulated by WT1. These results provide novel clues in our understanding of normal glomerular function and early events involved in glomerulosclerosis. Experiment Overall Design: Isolation of glomeruli from mutant (FVB-N4 Wt1+/R394W) and wild-type (FVB-N4 Wt1+/+) was performed after cardiac Dynabead perfusion. GeneChip analysis of glomeruli from 5 Wt1+/R394W mice and 5 Wt1+/+ littermates (N4-FVB) were performed independently. Animals were unweaned 27-day-old males. The Wt1+/R394W mice used were showing little albuminuria (<3 ug/ul on Coomassie blue stained SDS-PAGE gel) and no evidence of mesangial lesions by light microscopy.
2009-10-09 | E-GEOD-18358 | biostudies-arrayexpress
Project description:Absence of WT1 during kidney organoid development from human induced pluripotent stem cells (iPSCs) induces hallmarks of Wilms tumorigenesis. To define underlying transcriptional alterations and similarities to human patients, we performed timecourse RNA-seq of kidney organoid development from control iPSCs (control, not edited) and in the absence of WT1. Two timepoints for knockout (KO) of WT1 were investigated: In iPSCs (KO in iPSCs), and between day 4 and day 7 of organoid formation (KO d4-7).
2021-08-01 | E-MTAB-9957 | biostudies-arrayexpress
Project description:Purpose: examination of gene expression and translation changes in immortalized human epithelial cells (hTERT-RPE-1) induced by PDCD4 siRNA-knockdown.
2020-01-20 | GSE138533 | GEO
Project description:Improving protein production in human embryonic kidney cells is important structural studies and antibody production. The use of small non-protein coding RNA, such as microRNA, has been an effective method for increasing protein expression. Our high-throughput human microRNA screen in HEK 293 cells previously identified miRNA 22-3p as a promising candidate for increasing the expression of luciferase, couple of membrane proteins and a secreted fusion protein. To explore the mechanisms of this increase in protein expression and to understand the intracellular events, we conducted a gene expression analysis of luciferase- expressing HEK 293 cells transfected with a mir-22-3p mimic and compared with cells transfected with a negative control. Following microarray analysis, down-regulated genes were identified and were cross-referenced with the predicted targets of mir-22-3p and with results from our previous high-throughput siRNA screen. By performing common seed analysis on the possible targets, the list was narrowed to two genes, HIPK1 and FRAT2. These two genes were validated as being involved in improving luciferase production using siRNA and qRT PCR.
2017-12-17 | GSE92599 | GEO