Similar Datasets
Project description:Zc3h10 controls pre-mRNA profile in preadipocytes
| PRJNA622579 | ENA
Project description:Mitochondria are the energy-generating hubs of the cell. In spite of considerable advances, our understanding of the factors that regulate the molecular circuits that govern mitochondrial function remains incomplete. Using a genome-wide functional screen, we have identified the poorly characterized protein Zinc finger CCCH-type containing 10 (Zc3h10) as regulator of mitochondrial physiology. We show that Zc3h10 is a nuclear RNA binding protein that controls the fate of Slc25a37 and Prelid3a mRNA transcripts, two nuclear-encoded mitochondrial proteins central for iron and cardiolipin homeostasis. Depletion of Zc3h10 results in mitochondrial dysfunction and reduced TCA cycle flux. Notably, we have identified a loss-of-function mutation of Zc3h10 in humans (Tyr105 to Cys105) that is associated with decreased mitochondrial function, increased body mass index, fat mass, fasting glucose and triglycerides. Cells from Cys105 homozygotes display alterations in Slc25a37 and Prelid3a levels and defects in mitochondrial iron and cardiolipin homeostasis that derive in mitochondrial dysfunction.
2023-05-22 | GSE99138 | GEO
Project description:Mitochondria are the energy-generating hubs of the cell. In spite of considerable advances, our understanding of the factors that regulate the molecular circuits that govern mitochondrial function remains incomplete. Using a genome-wide functional screen, we have identified the poorly characterized protein Zinc finger CCCH-type containing 10 (Zc3h10) as regulator of mitochondrial physiology. We show that Zc3h10 is a nuclear RNA binding protein that controls the fate of Slc25a37 and Prelid3a mRNA transcripts, two nuclear-encoded mitochondrial proteins central for iron and cardiolipin homeostasis. Depletion of Zc3h10 results in mitochondrial dysfunction and reduced TCA cycle flux. Notably, we have identified a loss-of-function mutation of Zc3h10 in humans (Tyr105 to Cys105) that is associated with decreased mitochondrial function, increased body mass index, fat mass, fasting glucose and triglycerides. Cells from Cys105 homozygotes display alterations in Slc25a37 and Prelid3a levels and defects in mitochondrial iron and cardiolipin homeostasis that derive in mitochondrial dysfunction.
2023-05-22 | GSE99137 | GEO
Project description:Mitochondria are the energy-generating hubs of the cell. In spite of considerable advances, our understanding of the factors that regulate the molecular circuits that govern mitochondrial function remains incomplete. Using a genome-wide functional screen, we have identified the poorly characterized protein Zinc finger CCCH-type containing 10 (Zc3h10) as regulator of mitochondrial physiology. We show that Zc3h10 is a nuclear RNA binding protein that controls the fate of Slc25a37 and Prelid3a mRNA transcripts, two nuclear-encoded mitochondrial proteins central for iron and cardiolipin homeostasis. Depletion of Zc3h10 results in mitochondrial dysfunction and reduced TCA cycle flux. Notably, we have identified a loss-of-function mutation of Zc3h10 in humans (Tyr105 to Cys105) that is associated with decreased mitochondrial function, increased body mass index, fat mass, fasting glucose and triglycerides. Cells from Cys105 homozygotes display alterations in Slc25a37 and Prelid3a levels and defects in mitochondrial iron and cardiolipin homeostasis that derive in mitochondrial dysfunction.
2023-05-22 | GSE99136 | GEO
Project description:Mitochondria are the energy-generating hubs of the cell. In spite of considerable advances, our understanding of the factors that regulate the molecular circuits that govern mitochondrial function remains incomplete. Using a genome-wide functional screen, we have identified the poorly characterized protein Zinc finger CCCH-type containing 10 (Zc3h10) as regulator of mitochondrial physiology. We show that Zc3h10 is upregulated during physiological mitochondriogenesis such as myoblasts differentiation into myotubes. Zc3h10 overexpression boosts mitochondrial function and promotes myoblasts differentiation. On the other hand, depletion of Zc3h10 results in impaired myoblasts differentiation, mitochondrial dysfunction, reduced expression of electron transport chain (ETC) subunits and blunted TCA cycle flux. Notably, we have identified a loss-of-function mutation of Zc3h10 in humans (Tyr105 to Cys105) that is associated with increased body mass index, fat mass, fasting glucose and triglycerides. Isolated peripheral blood mononuclear cells from Cys105 homozygotes display reduced oxygen consumption rate, some ETC subunit expression and decreased levels of some TCA cycle metabolites that derive in mitochondrial dysfunction. Finally, our study identifies Zc3h10 as a novel mitochondrial regulator.
2018-02-26 | GSE99102 | GEO
Project description:Mitochondria are the energy-generating hubs of the cell. In spite of considerable advances, our understanding of the factors that regulate the molecular circuits that govern mitochondrial function remains incomplete. Using a genome-wide functional screen, we have identified the poorly characterized protein Zinc finger CCCH-type containing 10 (Zc3h10) as regulator of mitochondrial physiology. We show that Zc3h10 is upregulated during physiological mitochondriogenesis such as myoblasts differentiation into myotubes. Zc3h10 overexpression boosts mitochondrial function and promotes myoblasts differentiation. On the other hand, depletion of Zc3h10 results in impaired myoblasts differentiation, mitochondrial dysfunction, reduced expression of electron transport chain (ETC) subunits and blunted TCA cycle flux. Notably, we have identified a loss-of-function mutation of Zc3h10 in humans (Tyr105 to Cys105) that is associated with increased body mass index, fat mass, fasting glucose and triglycerides. Isolated peripheral blood mononuclear cells from Cys105 homozygotes display reduced oxygen consumption rate, some ETC subunit expression and decreased levels of some TCA cycle metabolites that derive in mitochondrial dysfunction. Finally, our study identifies Zc3h10 as a novel mitochondrial regulator.
2018-03-06 | PXD008833 | Pride
Project description:Zc3h10 is a RNA binding protein able to control both mRNA and miRNA metabolism. Zc3h10 is ubiquitously expressed and controls both cell differentiation and energy metabolism. In this dataset, we include the expression data obtained adipocytes differentiated for nine days treated with scramble RNA (control) and a Zc3h10 specific shRNA. This data were used to verify which genes are differentially expressed by lack of Zc3h10 during adipogenesis.
2023-02-14 | GSE115913 | GEO
Project description:Using high throughput sequencing, we report Zc3h10 enrichment in promoter regions of of thermogenic genes.
2019-11-01 | GSE139029 | GEO
Project description:Zc3h10 controls mitochondrial function coupling iron and cardiolipin homeostasis.
| PRJNA387412 | ENA
Project description:Extracellular matrix (ECM) remodelling occurs during tissue repair and inflammation-related pathologies with deposition of specific proteins. White adipose tissue (WAT) was recently shown to be the site of substantial interstitial fibrosis. ECM components, such as fibronectin, and their receptors integrins control cell migration, proliferation and differentiation. Adipocyte differentiation which is under the control of a specific transcriptional network is associated with decrease of fibronectin-rich matrix. Considering macrophage accumulation in white adipose tissues from obese subjects, we recently demonstrated that macrophage-secreted factors provoke an inhibition of differentiation with a proinflammatory state of human preadipocytes. The functional analysis of gene expression measurements obtained from cDNA microarray experiments reveals that themes related to the “extracellular matrix” are among the most significantly enriched in overexpressed genes in inflammatory preadipocytes. ECM remodelling, characterized by high deposition of fibronectin, collagen I and tenascin-C and important clustering of ECM receptors integrin alpha-5, is associated with increased proliferation and migration of preadipocytes. siRNA deletion of NF-kappaB in inflammatory preadipocytes decreased fibronectin network formation and their proliferation. Cyclin D1 and FAK constitute pivotal molecular targets in the synergistic promotion of migration and proliferation of the inflammatory preadipocytes. Importantly, interactions between preadipocytes and macrophages are favoured in 3D collagen I, a microenvironment mimicking fibrosis context of obese WATs. These data suggest that inflammatory preadipocytes could contribute to the production of fibrosis components and, in the context of WAT repair, these altered properties of preadipocytes could further lead to reconstitution of new fat clusters. Keywords: cell type comparison
2007-09-24 | GSE9017 | GEO