Gene expression analysis of F9 cells double knock-down for Sox7 and Sox17
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE43232 | GEO | 2013/04/23
SECONDARY ACCESSION(S): PRJNA185341
REPOSITORIES: GEO
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Project description:Analysis of the expression of F9 cells after knockdown of Sox7 and Sox17 during their primitive endoderm differnetiation induction with retinoic acid. Results provide information on the endodermal gene expression program regulated by Sox7 and Sox17. Sox7 Sox17 double KD vs. control in F9 cells
2013-04-23 | E-GEOD-43232 | biostudies-arrayexpress
Project description:This study aimed to understand the transcriptional networks regulating endoderm specification from HESC and therefore explored the phenotype of CA1 and CA2 HESC constitutively over-expressing SOX7 or SOX17. Cell lines were created using an inducible construct whereby clonal populations containing transgene integration are selected by Neomycin resistance without expressing of the gene of interest (NoCre controls). Transgene expression is induced via Cre-mediated recombination and selected for puromycin resistance (SOX O/E). The phenotype of the resulting cells suggests that SOX7 expressing HESC represent stable extraembryonic endoderm progenitors, while SOX17 expressing HESC represent early definitive endoderm progenitors. Both in vitro and in vivo SOX7 expressing HESC are restricted to the extraembryonic endoderm lineage, while SOX17 expressing HESC demonstrate mesendodermal specificity. In vitro, SOX17 expressing HESC efficiently produce mature definitive endoderm derivatives. The molecular phenotype of the resulting SOX7 and SOX17 expressing HESC was characterized by microarray analysis Experiment Overall Design: Total RNA was extracted from confluent monolayer cultures of SOX7 over-expressing HESC, SOX17 over-expressing HESC, and their respective control parental HESC lines (designated NoCre Sox7 and NoCre Sox17).
2008-10-20 | E-GEOD-10809 | biostudies-arrayexpress
Project description:This study aimed to understand the transcriptional networks regulating endoderm specification from HESC and therefore explored the phenotype of CA1 and CA2 HESC constitutively over-expressing SOX7 or SOX17. Cell lines were created using an inducible construct whereby clonal populations containing transgene integration are selected by Neomycin resistance without expressing of the gene of interest (NoCre controls). Transgene expression is induced via Cre-mediated recombination and selected for puromycin resistance (SOX O/E). The phenotype of the resulting cells suggests that SOX7 expressing HESC represent stable extraembryonic endoderm progenitors, while SOX17 expressing HESC represent early definitive endoderm progenitors. Both in vitro and in vivo SOX7 expressing HESC are restricted to the extraembryonic endoderm lineage, while SOX17 expressing HESC demonstrate mesendodermal specificity. In vitro, SOX17 expressing HESC efficiently produce mature definitive endoderm derivatives. The molecular phenotype of the resulting SOX7 and SOX17 expressing HESC was characterized by microarray analysis Keywords: cell line comparison
2008-08-11 | GSE10809 | GEO
Project description:To find out the target of transcription factor Sox7 and Sox17, DNA microarray analysis was performed with RNA from Sox7 and Sox17 knockdown HUVECs.
2016-11-23 | GSE75380 | GEO
Project description:Glioblastoma multiforme (GBM) is a highly aggressive and vascularized malignant brain tumor. SoxF transcription factors consisting of Sox7, Sox17, and Sox18 are expressed specifically in endothelial cells (ECs) and contribute to vascular morphogenesis. While the role of Sox17 was found in subcutaneous ectopic tumors, Sox7 has not been studied in the context of tumor angiogenesis. Here, we investigated gene expression profile of RNA analysis of Sox7- and Sox17-deficient mouse endothelial cells from high grade glioma using RNA sequencing to validate molecular characteristics of Sox7 and Sox17 in high grade glioma.
2018-01-27 | GSE107530 | GEO
Project description:To understand the role of Sox7 in primitive endoderm differentiation, we compare the gene expression pattern of Sox7 (+/-) and Sox7 (-/-) ES cells with or without dexamethasome (Dex) treatment. Because these ES cells harbour Gata6-GR transgene, Dex treatment forces ES cells differentate into XEN-like cells. As Sox7 (-/-) ES cells can differentiate into XEN-like cell by morphology, we assessed genome wide gene expression pattern.
2015-09-14 | GSE66971 | GEO
Project description:To understand the role of Sox7 in primitive endoderm differentiation, we compare the gene expression pattern of Sox7 (+/-) and Sox7 (-/-) ES cells with or without dexamethasome (Dex) treatment. Because these ES cells harbour Gata6-GR transgene, Dex treatment forces ES cells differentate into XEN-like cells. As Sox7 (-/-) ES cells can differentiate into XEN-like cell by morphology, we assessed genome wide gene expression pattern. Sox7 (+/-) ES cells and Sox7 (-/-) ES cells are forced to differentiate into XEN-like cells by Gata6-GR transgene. To compare the gene expression, we collected RNA samples at day4 with or without dexamethasone treatment from each genotype.
2015-09-14 | E-GEOD-66971 | biostudies-arrayexpress
Project description:Cardiac muscle differentiation in vivo is guided by sequential growth factor signals, including endoderm-derived diffusible factors, impinging on cardiogenic genes in the developing mesoderm. Previously, by RNA interference in AB2.2 mouse embryonic stem cells (mESCs), we identified the endodermal transcription factor Sox17 as essential for Mesp1 induction in primitive mesoderm and subsequent cardiac muscle differentiation. However, downstream effectors of Sox17 remained to be proven functionally. In this study, we used genome-wide profiling of Sox17-dependent genes in AB2.2 cells, RNA interference, chromatin immunoprecipitation, and luciferase reporter genes to dissect this pathway. Sox17 was required not only for Hhex (a second endodermal transcription factor) but also for Cer1, a growth factor inhibitor from endoderm that, like Hhex, controls mesoderm patterning in Xenopus toward a cardiac fate. Suppressing Hhex or Cer1 blocked cardiac myogenesis, although at a later stage than induction of Mesp1/2. Hhex was required but not sufficient for Cer1 expression. Over-expression of Sox17 induced endogenous Cer1 and sequence-specific transcription of a Cer1 reporter gene. Forced expression of Cer1 was sufficient to rescue cardiac differentiation in Hhex-deficient cells. Thus, Hhex and Cer1 are indispensable components of the Sox17 pathway for cardiopoiesis in mESCs, acting at a stage downstream from Mesp1/2. Keywords: Cardiac development, Embryonic stem cells, Endoderm, Myogenesis, RNA interference Genome-wide expression profiling of Sox17-dependent genes. Mouse embryonic stem cells expressing Sox17 or luciferase shRNA were differentiated for up to 10 days by the embryoid body method [PMID:8155574], then were analysed using Affymetrix microarrays. ESCs were transduced with lentiviral vectors coexpressing enhanced green fluorescent protein (eGFP) with shRNA against Sox17, or against firefly luciferase. Transduced cells were flow-sorted based on GFP fluorescence, grown as embryoid bodies, and transferred to tissue culture plates after 4.5 days [PMID:17360443]. Cells were harvested at days 0, 2, 4, 5, 6, 8 and 10 in two biological replicates, except where noted.
2015-07-30 | E-GEOD-71528 | biostudies-arrayexpress
Project description:Cardiac muscle differentiation in vivo is guided by sequential growth factor signals, including endoderm-derived diffusible factors, impinging on cardiogenic genes in the developing mesoderm. Previously, by RNA interference in AB2.2 mouse embryonic stem cells (mESCs), we identified the endodermal transcription factor Sox17 as essential for Mesp1 induction in primitive mesoderm and subsequent cardiac muscle differentiation. However, downstream effectors of Sox17 remained to be proven functionally. In this study, we used genome-wide profiling of Sox17-dependent genes in AB2.2 cells, RNA interference, chromatin immunoprecipitation, and luciferase reporter genes to dissect this pathway. Sox17 was required not only for Hhex (a second endodermal transcription factor) but also for Cer1, a growth factor inhibitor from endoderm that, like Hhex, controls mesoderm patterning in Xenopus toward a cardiac fate. Suppressing Hhex or Cer1 blocked cardiac myogenesis, although at a later stage than induction of Mesp1/2. Hhex was required but not sufficient for Cer1 expression. Over-expression of Sox17 induced endogenous Cer1 and sequence-specific transcription of a Cer1 reporter gene. Forced expression of Cer1 was sufficient to rescue cardiac differentiation in Hhex-deficient cells. Thus, Hhex and Cer1 are indispensable components of the Sox17 pathway for cardiopoiesis in mESCs, acting at a stage downstream from Mesp1/2. Keywords: Cardiac development, Embryonic stem cells, Endoderm, Myogenesis, RNA interference
2015-07-30 | GSE71528 | GEO
Project description:Using homologous recombination in human ESC, we inserted an enhanced green fluorescent protein (eGFP) transgene into a locus encoding a postulated marker of human endoderm, SOX17 in H9 human embryonic stem cells. This allowed purification of SOX17+ hESC endodermal progeny by fluorescence activated cell sorting (FACS) to generate microarray gene expression profile.
2011-03-15 | GSE26862 | GEO