SOX11-deficiency causes schizophrenia through disturbing progenitor polarity and disrupting mossy fiber projections in the hippocampus
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ABSTRACT:
PROVIDER: PRJNA666462 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12744500_1.fastq.gz | Fastqsanger.gz | |||
| SRR12744500_2.fastq.gz | Fastqsanger.gz | |||
| SRR12744495_1.fastq.gz | Fastqsanger.gz | |||
| SRR12744495_2.fastq.gz | Fastqsanger.gz | |||
| SRR12744496_1.fastq.gz | Fastqsanger.gz |
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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.
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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.
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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.
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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.
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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.
2013-07-11 | GSE44308 | GEO
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.
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Project description:In this study, we demonstrated that baseline SOX11 expression was significantly higher in dermal fibroblasts (DFs) isolated from patients with SSc than that in controls, and increased in response to TGF-b. We then showed that SOX11 is involved in the expression of periostin and some periostin-dependent fibrotic factors identified in lung fibroblasts previously. Moreover, we identified some fibrotic factors induced by SOX11 in DNA microarrays combining TGF-b induction and SOX11 knockdown. Finally, we showed that genetic deletion of SOX11 in Postn positive fibroblast cells protects from bleomycin (BLM)-induced skin fibrosis. Altogether, our data indicate that SOX11 and periostin forms a vicious circle and that TGF-b activates this circle specifically in SSc dermal fibroblasts.
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