Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1136072 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29844952_1.fastq.gz | Fastqsanger.gz | |||
| SRR29844952_2.fastq.gz | Fastqsanger.gz | |||
| SRR29844953_1.fastq.gz | Fastqsanger.gz | |||
| SRR29844953_2.fastq.gz | Fastqsanger.gz | |||
| SRR29844954_1.fastq.gz | Fastqsanger.gz |
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Project description:m6A regulates virtually every step in RNA metabolism. However, its toles in limb development remains largely unknown. To understand the roles, we created a limb bud-specific conditional knockout (cKO) mice and control heterozygous (cHet) mice of the Mettl14 gene, which encodes an essential subunit in the m6A methyltransferase complex METTL3/METTL14. We harvested limb buds from the mice on E12.5 and applied the proteins to quantitative mass spectrometry to understand how the depletion of Mettl14 affected the proteomes.
2025-04-03 | PXD049092 | Pride
Project description:The purpose of this project is to explore the changes in signaling pathways after Mettl3 knockout, and to identify potential downstream target proteins of Mettl3 along with the signaling pathways they are involved in. Ultimately elucidating the molecular mechanisms underlying Mettl3 pathogenesis. Retina of control and Mettl3 knockout mice were collected, and samples were then used for proteomic analysis. After tissue collection, a series of cutting-edge technologies, including protein extraction, enzyme digestion, liquid chromatography-tandem mass spectrometry, and bioinformatics analysis, were employed to investigate the quantitative proteome of the samples.
2024-10-12 | PXD056750 | Pride
Project description:We performed gene expression profiling by microarray using RNA extracted from healthy free wall left ventricle tissues from control and Hira cardiomyocyte-specific conditional knockout mice at 6 weeks of age. Hira is a histone chaperone responsible for replication-independent incorporation of histone variant H3.3 at actively transcribed regions. Conditional knockout of Hira in cardiomyocytes resulted in impaired cardiac function, cardiomyocyte degeneration and focal replacement fibrosis. These results illustrate the role of Hira in controlling the cardiac gene program. 4 animals per group (control and Hira conditional knockout) hybridized in triplicate. RNA was extracted from healthy free wall left ventricle.
2016-04-06 | E-GEOD-71833 | biostudies-arrayexpress
Project description:N6-methyladenosine (m6A) is the most common epigenetic modification of RNA, but whether m6A RNA methylation modulates cardiovascular development or congenital heart diseases (CHDs) has not been determined. The published high-throughput sequencing data suggested that transcripts of genes related to CHDs were prone to m6A modification, while the expression of methyltransferase-like 3 (METTL3)-involved methyltransferase complex was downregulated in mouse embryonic hearts following prenatal alcohol exposure as a critical CHD risk factor, indicating the association of insufficient m6A RNA methylation with CHDs. Using cardiovascular-specific Mettl3 knockout mice (Tagln-Cre; Mettl3flox/flox), we observed that cardiovascular Mettl3 deficiency resulted in postnatal lethality and profound congenital cardiac defects, including left pulmonary stenosis, ventricular septal defects and right ventricular hypoplasia. The m6A-specific methylated RNA-immunoprecipitation sequencing identified Sox4, Sox11 and Mef2a, the critical transcription factors involved in right ventricle and outflow tract development, were the regulatory targets of METTL3-catalyzed m6A RNA methylation. Mettl3 deficiency-caused insufficient m6A RNA methylation downregulated the expression of SOX4, SOX11 and MEF2A in mouse embryonic hearts. In conclusion, cardiovascular Mettl3 deficiency directly led to congenital cardiac defects by downregulating the m6A-dependent expression of Mef2a, Sox4 and Sox11. METTL3-catalyzed m6A RNA methylation may become a potential target for the prevention and treatment of CHDs.
2025-05-07 | GSE288034 | GEO
Project description:RNA sequencing of primary hepatocytes from Control and and hepatocyte-specific Mettl3 knockout with ALB-Cre (Mettl3 cKO) mice after Actinomycin D treatment.
2022-05-26 | GSE198513 | GEO
Project description:RNA sequencing of livers tissues from control and hepatocyte-specific Mettl3 knockout with ALB-Cre (Mettl3 cKO) mice at different time points after birth.
2022-05-26 | GSE198512 | 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:To investigate the effect of Mettl3 in the uterus, we generated mice with conditional ablation of Mettl3 in progesterone receptor (PR)–positive cells (PgrCre Mettl3 fl/fl). And the uterus of Mettl3 cKO and control mice on GD4 were obtained for RNA-seq analysis.
2023-09-07 | GSE208096 | GEO