Expression data from dissected caudal area of urogenital ridges of Sox11 knockout and wildtype E10.75 mouse embryos
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ABSTRACT:
PROVIDER: PRJNA415168 | ENA |
REPOSITORIES: ENA
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Project description:The transcription factor Sox11 is a crucial regulator of kidney development. It is expressed in both mesenchymal and epithelial components of the early kidney anlagen. Deletion of Sox11 in mice causes an extension of the domain expressing Gdnf within rostral regions of the nephrogenic cord and results in duplex kidney formation. To gain insight into potential targets we performed microarray analysis on RNA isolated from the caudal region of E10.75 wildtype and mutant nephrogenic cords. 281 probe sets presented statistically significant changes (76 up, 205 down; FDR<0.1)
2017-12-31 | GSE105426 | GEO
Project description:The Wilms tumor protein Wt1 is a transcription factor known to play an important role in urogenital development. Mutations in the human Wt1 encoding gene (WT1) lead to several syndromes associated with defective renal and sexual development, namely WAGR-, Denys-Drash-, and Frasier-syndrome. During mammalian embryogenesis, urogenital development starts with formation of the urogenital ridges, consisting of the embryonic kidneys, called mesonephroi, and the gonads. In Wt1 knockout mice, these ridges start to form, degenerate, however, during further embryonic development . Although WT1 and the syndromes associated with its mutation are known for several years, it is still unclear which genes, regulated by Wt1, mediate the whole variety of Wt1's function in gonad and mesonephros development. To obtain a comprehensive view on Wt1-dependent gene activity in developing urogenital ridges, we employed microarray analysis. Comparison of gene expression in Wt1 wild-type and knockout mice, led to the identification of almost 150 genes with differences in expression levels higher than factor three. Keywords: wild-type and knockout comparison
2007-06-01 | GSE6700 | GEO
Project description:SOX11 pioneer transcription factor is aberrantly expressed, it has an oncogenic role and its overexpression associates with worse prognosis in patients with mantle cell lymphomas (MCL). Using a proximity labeling (BioID2)/Mass Spectrometry-based proteomic strategyies, we identified SMARCA4, the central catalytic subunit of the SWI/SNF chromatin-remodeling complex, as one of the most significant SOX11-specific interacting proteins. SMARCA4 expression is directly regulated by SOX11, and its upregulation is associated with worse overall survival in patients with MCL, independently of other high-risk factors. Integration of global DNA-binding and transcriptomic profiles revealed that SOX11 and SMARCA4 share 60% specific peaks, predominantly in promoter regions. Disruption of SOX11:SMARCA4 interaction via SOX11 knockout or SMARCA4 PROTAC-degradation significantly reduced co-occupancy and co-targeted gene expression, including key BCR signaling pathway components. Our results suggest that SOX11:SMARCA4 complex binds to common regulatory sequences enabling the accession to chromatin and transcriptomic regulation of key oncogenic pathways for the development of MCL pathogenesis.
2025-08-04 | PXD051143 | Pride
Project description:The neural transcription factor SOX11 is overexpressed in aggressive lymphoid neoplasms mainly in mantle cell lymphoma (MCL). We have recently demonstrated SOX11 tumorigenic potential in vivo by showing a significant reduction on tumor growth of SOX11-knockdown MCL cells in xenograft experiments, confirming the clinical observations that SOX11 may play an important role in the aggressive behavior of MCL (Vegliante et al., 2013). However, the specific mechanisms regulated by SOX11 that promote the oncogenic and rapid tumor growth of aggressive MCL still remain to be elucidated. To further characterize the potential oncogenic mechanisms regulated by SOX11 in MCL, we have analyzed the GEP derived from the xenograft SOX11-positive and knockdown xenograft derived tumors. Differential gene expression between SOX11-positive Z138 and SOX11-negative Z138 MCL cell lines xenotransplanted in SCID mices derived tumors.
2014-11-04 | GSE52892 | GEO
Project description:The neural transcription factor SOX11 is overexpressed in aggressive lymphoid neoplasms mainly in mantle cell lymphoma (MCL). We have recently demonstrated SOX11 tumorigenic potential in vivo by showing a significant reduction on tumor growth of SOX11-knockdown MCL cells in xenograft experiments, confirming the clinical observations that SOX11 may play an important role in the aggressive behavior of MCL (Vegliante et al., 2013). However, the specific mechanisms regulated by SOX11 that promote the oncogenic and rapid tumor growth of aggressive MCL still remain to be elucidated. To further characterize the potential oncogenic mechanisms regulated by SOX11 in MCL, we have analyzed the GEP derived from the xenograft SOX11-positive and knockdown xenograft derived tumors. Differential gene expression between SOX11-positive Z138 and SOX11-negative Z138 MCL cell lines xenotransplanted in SCID mices derived tumors. To determine the transcriptional programs regulated by SOX11 we first generated a MCL cellular model with reduced SOX11 protein levels by infecting MCL cell lines with lentiviral particles carrying shRNA plasmids specifically targeting SOX11 (shSOX11.1 and shSOX11.3). Next, CB17-severe combined immunodeficient (CB17-SCID) mice (Charles River Laboratory, Wilmington, MA) were subcutaneously inoculated into their lower dorsum with Z138 shSOX11.1, shSOX11.3, shControl in Matrigel basement membrane matrix and compared the GEP of SOX11-positive and SOX11-negative MCL xenotransplant derived tumors using the Affymetrix U133+2.0 microarrays.
2014-11-04 | E-GEOD-52892 | biostudies-arrayexpress
Project description:The vertebrate enteric nervous system (ENS) is derived from vagal neural crest cells, which enter the foregut as progenitors that migrate from rostral to caudal to populate the entire length of the gut. Here, we show that transcription factors sox11a and sox11b, zebrafish orthologs of the human sox11 gene, are highly expressed in neural crest cells transitioning from progenitors to differentiating neuronal subtypes. Accordingly, CRISPR-Cas9 depletion shows that loss of sox11 paralogs reduces the number of neurons that express the inhibitory motor neuron marker adcyap1b without affecting cell proliferation or death. Transcription factor footprinting analysis of open chromatin regions identified by ATAC-seq reveals sox11 binding sites in the adcyap1b enhancer. Furthermore, mutational analysis shows these binding sites are required for mediating enhancer-driven reporter expression. Taken together, our results demonstrate an important and previously unrecognized role for sox11a and sox11b in neuronal subtype specification in the developing zebrafish ENS.
2025-07-23 | GSE303101 | GEO
Project description:We analyzed global mRNA expression in urogenital ridges of embryos that were either heterozygous for the MM-CM-<llerian Inhibiting Substance type II receptor or homozygously deleted to study the genes regulated by MIS during MM-CM-<llerian duct regression. Approximately 200 mosue embryos were sorted for heterozygous or homozygous deletion of the MISR2, urogenital ridges were collected and the gonads were discarded. mRNA was prepared from pooled ridges and sent for Affymetrix analysis.
2013-05-01 | E-GEOD-38009 | biostudies-arrayexpress
Project description:The neural transcription factor SOX11 is overexpressed in aggressive lymphoid neoplasms mainly in mantle cell lymphoma (MCL), but its functional role in malignant B-cells is unknown. To identify target genes transcriptionally regulated by SOX11 in malignant lymphoid cells, we have used Gene Expression Profiling (GEP) after SOX11 silencing in MCL cell lines.
2013-04-04 | GSE34763 | GEO
Project description:The neural transcription factor SOX11 is overexpressed in aggressive lymphoid neoplasms mainly in mantle cell lymphoma (MCL), but its functional role in malignant B-cells is unknown. To identify target genes transcriptionally regulated by SOX11 in malignant lymphoid cells, we have used Gene Expression Profiling (GEP) after SOX11 silencing in MCL cell lines. Differential gene expression between Z138-shSOX11 and Z138-shControl MCL cell lines. To determine the transcriptional programs regulated by SOX11, we first generated an MCL cellular model with reduced SOX11 protein levels by infecting MCL cell lines with lentiviral particles carrying shRNA plasmids specifically targeting SOX11 (shSOX11.1 and shSOX11.3). Next, we compared the GEP of shSOX11 and shControl Z138 stable transduced clones using the Affymetrix U133+2.0 microarrays.
2013-04-04 | E-GEOD-34763 | biostudies-arrayexpress