Sox11 loss-of-function mutant cortex at E17.5
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE44308 | GEO | 2013/07/11
SECONDARY ACCESSION(S): PRJNA189410
REPOSITORIES: GEO
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Project description:Expression profiling of cortex from embryonic day (E) 17.5 telencephalon of Sox11(+/+) and Sox11(-/-) mouse embryos. Sox11 is implicated in regulating proliferation, neuronal migration and differentiation. We used microarray to identify genes that were differentially expressed in the cortex in the wild type and Sox11 knockout embryos at E17.5. To uncover the molecular mechanisms undelying the function of Sox11 in cortical development, we conducted microarray analysis of E17.5 cortices from wild type and Sox11(-/-) mice. Total RNA was isolated from the cortex of one wild type embryo and one Sox11(-/-) littermate at E17.5. cRNA probe synthesis, hybridization, scanning, and data collection were performed following the manufacturer's instruction.
2013-07-11 | E-GEOD-44308 | biostudies-arrayexpress
Project description:Since Usp11 encodes a DUB, we reasoned that Usp11 deficiency may lead to increased ubiquitination and destabilization of a protein that functions in neuronal differentiation and migration.To define the molecular mechanism of Usp11 deficiency on cortical development, we performed a label-free quantitative liquid chromatography-tandem Mass Spectrometry (LC-MS/MS) analysis to detect the protein expression profiles in E17.5 WT and Usp11 KO cortices in four biological repeats.
2021-01-29 | PXD021587 | 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 Insm1 gene encodes a zinc finger factor expressed in many endocrine organs. We show here that Insm1 is required for differentiation of all endocrine cell types in the pituitary. Thus, in Insm1 mutant mice, hormones characteristic of the different pituitary cell types (thyroid, follicle and melanocyte stimulating hormone, adrenocorticotrope hormone, growth hormone and prolactin) are absent or produced at markedly reduced levels. The differentiation deficit is accompanied by an up-regulated expression of components of the Notch signaling pathway. Further, skeletal muscle-specific genes are ectopically expressed, indicating that Insm1 blocks a muscle-specific expression program. Since Insm1 is also essential for differentiation of endocrine cells in the pancreas, intestine and adrenal gland, it is emerging as a transcription factor that acts in a pan-endocrine manner. The Insm1 factor contains a SNAG domain at its N-terminus, and we show here that the SNAG domain recruits histone modifying factors (Kdm1a, Hdac1/2 and Rcor1-3) and other proteins implicated in transcriptional regulation (Hmg20a/b and Gse1). Deletion of the SNAG domain in mice disrupted differentiation of pituitary endocrine cells, and resulted in an upregulated expression of components of the Notch signaling pathway and ectopic expression of skeletal muscle-specific genes. Our work demonstrates that Insm1 acts in the transcriptional network that controls differentiation of endocrine cells in the anterior pituitary gland, and requires the SNAG domain to exert this function in vivo. Analysis of genes regulated by Insm1 in embryonic day 17.5 pituitary gland. Total RNA from pituitary glands of E17.5 control embryos was compared to E17.5 Insm1 mutant embryos.
2013-10-20 | E-GEOD-46139 | 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:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare transcriptome profiling (RNA-seq) of E17.5 cortexes of offspring from control and preeclampsia mother mice. Methods: E17.5 cortex mRNA profiles of offspring from control and preeclampsia mother mice were generated by deep sequencing, in triplicate, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. Results: Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (build mm9) and identified 16,014 transcripts in the E17.5 cortexes of offspring from control and preeclampsia mother mice with BWA workflow and 34,115 transcripts with TopHat workflow. R Conclusions: Our study represents the first detailed analysis of E17.5 cortical transcriptomes, with biologic replicates, generated by mRNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. Our results show that NGS offers a comprehensive and more accurate quantitative and qualitative evaluation of mRNA content within tissue. We conclude that mRNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.
2023-06-06 | GSE167193 | 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
Project description:To identify potential SOX11 target genes in myxoid liposarcoma (MLS) we stably transfected codon optimized full-length human SOX11 into the SOX11 negative MLS cell line MLS-1765. An emtpy vector (EV) was used as control. Potential SOX11 target genes were correlated with data set GSE52390.
2017-01-31 | GSE85231 | GEO