The human gene FOXM1 promotes cortical folding and improves learning and memory ability in mice [P0]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA608757 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11182800_1.fastq.gz | Fastqsanger.gz | |||
| SRR11182800_2.fastq.gz | Fastqsanger.gz | |||
| SRR11182799_1.fastq.gz | Fastqsanger.gz | |||
| SRR11182799_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 4 of 4 |
Similar Datasets
Project description:Purpose: To gain further insight into how FOXM1 causes generation of cortical expansion and folding in mice, single cell RNA-seq was used to analyze the cell type changes resulting from the cerebral cortices of P0 FOXM1 conditional knock in mice and littermate wild-type. Methods: Single cell isolation was prepared from P0 telencephalic tissue of wild-type (WT) and FOXM1f/+;Nestin-Cre mice. The fragmented cDNAs containing barcode and UMI sequences was built the library. Agilent 2100 Bioanalyzer was used to quality controlled and quantified. Single cell RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics. Results: Clustering and labeling of these cells visualized on a t-SNE plot between the wild-type (WT) and FOXM1f/+;Nestin-Cre mice brain cortex. Conclusions: Single cell RNA-seq data would provide an overall understanding how FOXM1 gene contribute to generation of cortical expansion and folding in mice.
2020-02-26 | GSE145934 | GEO
Project description:The human gene FOXM1 promotes cortical folding and improves learning and memory ability in mice
| PRJNA609350 | ENA
Project description:The human gene FOXM1 promotes cortical folding and improves learning and memory ability in mice [E15]
| PRJNA606257 | ENA
Project description:Purpose: To gain futher insight into how FOXM1 regulates the proliferative of neural progenitors ,RNA-seq was used to analyze the genome-wide changes resulting from the cerebral cortices of E15 FOXM1 conditional knock in mice and littermate wild-type. Methods: Total RNA from E15 telencephalic tissue of wild-type(WT) and FOXM1f/+;Nestin-Cre mice was extracted. Specifically, Agilent 2100 Bioanalyze was used to quality controlled and quantified. then, total RNA was converted to cDNA and bound the library. RNA-sequencing analysis was used by the Illumina HiSeq 2500 platform in Annoroad Genomics Results: Approximately one thousand transcripts showed differential expression between the wild-type(WT) and FOXM1f/+;Nestin-Cre mice brain cortex, with a fold change ≥1.5 and p value <0.05.Geneontology analysis of the up-regulated genes showed obvious enrichment of biological processes related to development and proliferation.The down-regulated genes exhibited enrichment of biological processes related to the negative regulation of cell proliferation and developmental process. These results reflected human FOXM1 plays a role in cortex development. Conclusions: RNA-seq based transcriptome characterization would provide a overall understanding how FOXM1 gene contribute to brain cortical development.
2020-02-13 | GSE145169 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2020-02-28 | GSE146130 | GEO
Project description:Aims: Cardiac fibroblasts (CFs) play a crucial role in cardiac remodelling, which is a common cause of heart failure (HF). However, the molecular mechanisms underlying the fibroblast-to-myofibroblast transition remain largely unknown. Foxm1 is well known in various cardiopulmonary pathologies. However, Foxm1-driven CF activation in the progression of cardiac remodelling to HF remains to be investigated. Methods: Changes in Foxm1 expression were assessed in samples from patients with HF and mice with transverse aortic constriction (TAC)-induced cardiac remodelling. Pharmacologic antagonist FDI-6 was used to explore the effects of Foxm1 inhibition on post-TAC outcomes. Tcf21-Cre and PostnMCM were used to evaluate Foxm1 loss- and gain-of-function in CFs and myofibroblasts, respectively. Cardiac function and remodelling were examined by echocardiography and histological analysis. Foxm1 downstream target genes were identified by mass spectrometry (MS) and transcriptomic analysis. Post-translational regulation was evaluated by in vitro chromatin immunoprecipitation, co-immunoprecipitation, and ubiquitination assays. Pharmacological inhibition of Usp10 or knockout of p38γ in vivo verified the signalling pathway by which Foxm1 regulated cardiac remodelling. Results: Foxm1 was upregulated in human HF samples as well as in the mouse cardiac remodelling model. CFs were the primary cell type responsible for Foxm1 upregulation. Foxm1 pharmacological inhibition or genetic knockout in CFs or myofibroblasts significantly attenuated TAC-induced cardiac remodelling and HF. Conversely, conditional overexpression of Foxm1 in CFs or myofibroblasts resulted in more severe pathological cardiac remodelling and dysfunction. Combined RNA-sequencing and MS analysis revealed that Foxm1 promoted Usp10 expression by binding to its promoter. Usp10 interacted with p38γ, resulting in p38γ deubiquitination and thus influencing the downstream p38 mitogen-activated protein kinase (MAPK) signalling pathway. Pharmacological inhibition of Usp10 or genetic knockout of p38γ ameliorated the exacerbated TAC-induced cardiac remodelling in mice with myofibroblast-specific Foxm1 overexpression. Conclusion: Our findings reveal an essential role of Foxm1 in CF activation during cardiac remodelling. These results suggest that targeting the Foxm1/Usp10/p38γ MAPK axis may represent a new potential therapeutic strategy against pathological cardiac remodelling and HF.
2024-03-10 | PXD050300 | Pride
Project description:Aims: Cardiac fibroblasts (CFs) play a crucial role in cardiac remodelling, which is a common cause of heart failure (HF). However, the molecular mechanisms underlying the fibroblast-to-myofibroblast transition remain largely unknown. Foxm1 is well known in various cardiopulmonary pathologies. However, Foxm1-driven CF activation in the progression of cardiac remodelling to HF remains to be investigated. Methods: Changes in Foxm1 expression were assessed in samples from patients with HF and mice with transverse aortic constriction (TAC)-induced cardiac remodelling. Pharmacologic antagonist FDI-6 was used to explore the effects of Foxm1 inhibition on post-TAC outcomes. Tcf21-Cre and PostnMCM were used to evaluate Foxm1 loss- and gain-of-function in CFs and myofibroblasts, respectively. Cardiac function and remodelling were examined by echocardiography and histological analysis. Foxm1 downstream target genes were identified by mass spectrometry (MS) and transcriptomic analysis. Post-translational regulation was evaluated by in vitro chromatin immunoprecipitation, co-immunoprecipitation, and ubiquitination assays. Pharmacological inhibition of Usp10 or knockout of p38γ in vivo verified the signalling pathway by which Foxm1 regulated cardiac remodelling. Results: Foxm1 was upregulated in human HF samples as well as in the mouse cardiac remodelling model. CFs were the primary cell type responsible for Foxm1 upregulation. Foxm1 pharmacological inhibition or genetic knockout in CFs or myofibroblasts significantly attenuated TAC-induced cardiac remodelling and HF. Conversely, conditional overexpression of Foxm1 in CFs or myofibroblasts resulted in more severe pathological cardiac remodelling and dysfunction. Combined RNA-sequencing and MS analysis revealed that Foxm1 promoted Usp10 expression by binding to its promoter. Usp10 interacted with p38γ, resulting in p38γ deubiquitination and thus influencing the downstream p38 mitogen-activated protein kinase (MAPK) signalling pathway. Pharmacological inhibition of Usp10 or genetic knockout of p38γ ameliorated the exacerbated TAC-induced cardiac remodelling in mice with myofibroblast-specific Foxm1 overexpression. Conclusion: Our findings reveal an essential role of Foxm1 in CF activation during cardiac remodelling. These results suggest that targeting the Foxm1/Usp10/p38γ MAPK axis may represent a new potential therapeutic strategy against pathological cardiac remodelling and HF.
2024-03-03 | PXD050281 | Pride
Project description:FOXM1 is a key transcription factor regulating cell cycle progression, DNA damage response, and a host of other hallmark cancer features, but the role of the FOXM1 cistrome in driving estrogen receptor-positive (ER+) vs. ER- breast cancer clinical outcomes remains undefined. Chromatin immunoprecipitation sequencing (ChIP-Seq) coupled with RNA sequencing (RNA-Seq) analyses was used to identify FOXM1 target genes in breast cancer cells (MCF-7) where FOXM1 expression was either induced by cell proliferation or repressed by p53 upregulation.
2015-10-26 | E-GEOD-72977 | biostudies-arrayexpress
Project description:FOXM1 is a key transcription factor regulating cell cycle progression, DNA damage response, and a host of other hallmark cancer features, but the role of the FOXM1 cistrome in driving estrogen receptor-positive (ER+) vs. ER- breast cancer clinical outcomes remains undefined. Chromatin immunoprecipitation sequencing (ChIP-Seq) coupled with RNA sequencing (RNA-Seq) analyses was used to identify FOXM1 target genes in breast cancer cells (MCF-7) where FOXM1 expression was either induced by cell proliferation or repressed by p53 upregulation.
2015-10-26 | E-GEOD-73370 | biostudies-arrayexpress
Project description:Fork-head box protein M1 (FoxM1) is a transcription factor which plays critical roles in development and progression of multiple cancers, including human hepatocellular carcinoma (HCC). However, the regulatory mechanism of FoxM1 itself remains largely unclear. Here, we discovered a novel role of abnormal spindle-like microcephaly associated (ASPM) in HCC, which binds to FoxM1 protein and enhances its stability by preventing proteasome-mediated degradation. ChIP-sequencing data showed that ASPM and FoxM1 co-occupies on the promoter region of multiple genes to promote their transcriptions, leading to the enhancement of a FoxM1-driven oncogenic progression. Intriguingly, FoxM1 binds to the promoter region of ASPM and transcriptionally activates the ASPM expression. Furthermore, data from clinical samples showed that a higher co-expression of ASPM and FoxM1 significantly correlates with poor prognosis in HCC, indicating that a positive feedforward loop between ASPM and FoxM1 coordinately promotes the aggressive progression in HCC. Collectively, our study reveals that reciprocal regulation of ASPM and FoxM1 amplifies the oncogenic progression and emphasizes an ASPM-FoxM1 feedforward loop could be a potential biomarker and therapeutic target in HCC.
2024-11-01 | GSE218100 | GEO