Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA263168 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:MEFs were grown from WT and PDPN-deficient mouse embryos and gene expression was analyzed. The aim was to determine whether a lack of PDPN caused significant global changes in gene expression in primary fibroblasts. Here, we performed a microarray on WT and PDPN-deficient mouse embryonic fibroblasts to determine whether there were signficiant underlying changes in gene expression. Two replicates each of WT and PDPN KO MEFs from C57BL6/J mice
2014-10-07 | E-GEOD-62081 | biostudies-arrayexpress
Project description:MEFs were grown from WT and PDPN-deficient mouse embryos and gene expression was analyzed. The aim was to determine whether a lack of PDPN caused significant global changes in gene expression in primary fibroblasts. Here, we performed a microarray on WT and PDPN-deficient mouse embryonic fibroblasts to determine whether there were signficiant underlying changes in gene expression.
2014-10-07 | GSE62081 | GEO
Project description:The effect of Podoplanin (Pdpn) expression on the differential expression profile of RAW264.7 cells has been characterised in wildtype, Pdpn knockout cells and Pdpn overexpressed cells before and after H. pylori infection using 770 genes from the NanoString Mouse PanCancer Pathways Panel.
2020-05-28 | GSE151269 | GEO
Project description:Microarray analysis of gene expression in ATM-deficient MEFs
| PRJNA131505 | ENA
Project description:Total Gene expression analysis of H3f3b null and WT MEFs
| PRJNA156027 | ENA
Project description:The macrophage response to infected microbes is crucial for the development of life-threatening sepsis. However, the mechanisms underlying pathophysiological regulation of macrophage subsets during sepsis remain poorly understood. Here, we report a novel mechanism in which the adhesion and degranulation-promoting adapter protein (ADAP) is essential for priming macrophages to induce podoplanin (PDPN) in response to bacterial infection during sepsis. We showed that ADAP expression was robustly induced in macrophages following LPS stimulation and was associated with sepsis severity. Furthermore, PDPN failed to be upregulated in TLR4 stimulated macrophages deficient in ADAP. A distinct PDPNhi peritoneal macrophage (PM) subset, which exhibited an M2-like phenotype and enhanced phagocytic activity, was generated in WT but not in ADAP-deficient septic mice. The blockade of PDPNhi PMs mimicked the effect of ADAP deficiency, which exacerbated sepsis. Mechanistically, BTK-mediated ADAP Y571 phosphorylation worked together with mTOR to converge on STAT3 activation for the transactivation of the PDPN promoter. Moreover, agonist activation of STAT3 profoundly potentiated the PDPNhi PM subset generation and alleviated sepsis severity in mice. Together, our findings reveal a novel mechanism whereby ADAP resets macrophage function by controlling the TLR4-induced upregulation of PDPN as a host innate immune defense during sepsis.
2025-01-10 | GSE281052 | GEO
Project description:The macrophage response to infected microbes is crucial for the development of life-threatening sepsis. However, the mechanisms underlying pathophysiological regulation of macrophage subsets during sepsis remain poorly understood. Here, we report a novel mechanism in which the adhesion and degranulation-promoting adapter protein (ADAP) is essential for priming macrophages to induce podoplanin (PDPN) in response to bacterial infection during sepsis. We showed that ADAP expression was robustly induced in macrophages following LPS stimulation and was associated with sepsis severity. Furthermore, PDPN failed to be upregulated in TLR4 stimulated macrophages deficient in ADAP. A distinct PDPNhi peritoneal macrophage (PM) subset, which exhibited an M2-like phenotype and enhanced phagocytic activity, was generated in WT but not in ADAP-deficient septic mice. The blockade of PDPNhi PMs mimicked the effect of ADAP deficiency, which exacerbated sepsis. Mechanistically, BTK-mediated ADAP Y571 phosphorylation worked together with mTOR to converge on STAT3 activation for the transactivation of the PDPN promoter. Moreover, agonist activation of STAT3 profoundly potentiated the PDPNhi PM subset generation and alleviated sepsis severity in mice. Together, our findings reveal a novel mechanism whereby ADAP resets macrophage function by controlling the TLR4-induced upregulation of PDPN as a host innate immune defense during sepsis.
2025-01-10 | GSE281049 | GEO
Project description:The macrophage response to infected microbes is crucial for the development of life-threatening sepsis. However, the mechanisms underlying pathophysiological regulation of macrophage subsets during sepsis remain poorly understood. Here, we report a novel mechanism in which the adhesion and degranulation-promoting adapter protein (ADAP) is essential for priming macrophages to induce podoplanin (PDPN) in response to bacterial infection during sepsis. We showed that ADAP expression was robustly induced in macrophages following LPS stimulation and was associated with sepsis severity. Furthermore, PDPN failed to be upregulated in TLR4 stimulated macrophages deficient in ADAP. A distinct PDPNhi peritoneal macrophage (PM) subset, which exhibited an M2-like phenotype and enhanced phagocytic activity, was generated in WT but not in ADAP-deficient septic mice. The blockade of PDPNhi PMs mimicked the effect of ADAP deficiency, which exacerbated sepsis. Mechanistically, BTK-mediated ADAP Y571 phosphorylation worked together with mTOR to converge on STAT3 activation for the transactivation of the PDPN promoter. Moreover, agonist activation of STAT3 profoundly potentiated the PDPNhi PM subset generation and alleviated sepsis severity in mice. Together, our findings reveal a novel mechanism whereby ADAP resets macrophage function by controlling the TLR4-induced upregulation of PDPN as a host innate immune defense during sepsis.
2025-01-10 | GSE281047 | GEO
Project description:Introgressed variants from other species can be an important source of genetic variation because they may arise rapidly, can include multiple mutations on a single haplotype, and have often been pretested by selection in the species of origin. Although introgressed alleles are generally deleterious, several studies have reported introgression as the source of adaptive alleles-including the rodenticide-resistant variant of Vkorc1 that introgressed from Mus spretus into European populations of Mus musculus domesticus. Here, we conducted bidirectional genome scans to characterize introgressed regions into one wild population of M. spretus from Spain and three wild populations of M. m. domesticus from France, Germany, and Iran. Despite the fact that these species show considerable intrinsic postzygotic reproductive isolation, introgression was observed in all individuals, including in the M. musculus reference genome (GRCm38). Mus spretus individuals had a greater proportion of introgression compared with M. m. domesticus, and within M. m. domesticus, the proportion of introgression decreased with geographic distance from the area of sympatry. Introgression was observed on all autosomes for both species, but not on the X-chromosome in M. m. domesticus, consistent with known X-linked hybrid sterility and inviability genes that have been mapped to the M. spretus X-chromosome. Tract lengths were generally short with a few outliers of up to 2.7 Mb. Interestingly, the longest introgressed tracts were in olfactory receptor regions, and introgressed tracts were significantly enriched for olfactory receptor genes in both species, suggesting that introgression may be a source of functional novelty even between species with high barriers to gene flow.
| S-EPMC8784167 | biostudies-literature
Project description:Differential expression between FHL2-/- and WT MEFs.
| PRJNA107309 | ENA