Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1216165 | ENA |
REPOSITORIES: ENA
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Project description:Coxsackievirus A10 (CV-A10) infection, a prominent cause of childhood hand-foot-and-mouth disease (HFMD), frequently manifests with the intriguing phenomenon of onychomadesis, characterized by nail shedding. However, the underlying mechanism is elusive. Here, we found that CV-A10 infection in mice could suppress Wnt/β-catenin signaling by restraining LDL-receptor-related protein 6 (LRP6) phosphorylation and β-catenin accumulation and led to onychomadesis. Mechanistically, CV-A10 mimics Dickkopf-related protein 1 (DKK1) to interact with Kringle-containing transmembrane protein 1 (KRM1), the CV-A10 cellular receptor. We further found that Wnt agonist (GSK3β inhibitor) CHIR99021 can restore nail stem cell differentiation. These findings provide novel insights into the pathogenesis of CV-A10 and related viruses in onychomadesis and guide prognosis assessment and clinical treatment of the disease.
2024-04-08 | GSE261919 | GEO
Project description:Coxsackievirus A10 (CV-A10) infection, a prominent cause of childhood hand-foot-and-mouth disease (HFMD), frequently manifests with the intriguing phenomenon of onychomadesis, characterized by nail shedding. However, the underlying mechanism is elusive. Here, we found that CV-A10 infection in mice could suppress Wnt/β-catenin signaling by restraining LDL-receptor-related protein 6 (LRP6) phosphorylation and β-catenin accumulation and led to onychomadesis. Mechanistically, CV-A10 mimics Dickkopf-related protein 1 (DKK1) to interact with Kringle-containing transmembrane protein 1 (KRM1), the CV-A10 cellular receptor. We further found that Wnt agonist (GSK3β inhibitor) CHIR99021 can restore nail stem cell differentiation. These findings provide novel insights into the pathogenesis of CV-A10 and related viruses in onychomadesis and guide prognosis assessment and clinical treatment of the disease.
2025-03-31 | GSE212105 | GEO
Project description:Digital gene expression profiling (DGE) was used to compare the responses of Penicillium decumbens strains to different carbon sources including glucose, cellulose and cellulose-wheat bran. In both wild-type strain 114-2 and cellulase hyperproducing mutant JU-A10-T, transcription of lignocellulolytic enzymes were significantly up-regulated in the presense of cellulose. Relative to 114-2, coordinated up-regulation of lignocellulolytic enzymes and down-regulation of amylases and proteases were observed in JU-A10-T, especially in the cellulose-wheat bran medium. The expression of the principal β-glucosidase BGLI gene was not elevated in JU-A10-T, like the cellulases and hemicellulases, suggesting a different regulatory mechanism for this enzyme. Functional analysis of genes up-regulated in JU-A10-T relative to 114-2 also showed enrichment of proteins involved in amino acid synthesis, protein synthesis, and post-translational modification, compatible with the higher level of production of secreted proteins in JU-A10-T.
2013-01-18 | GSE34288 | GEO
Project description:Coxsackievirus A10 (CV-A10) constitutes one of the major pathogens of hand, foot, and mouth disease (HFMD), which can cause mild to severe illness and even death. Most of these severe and death cases were closely associated with their neurological impairments, but the underlying mechanism of neuropathological injury induced by CV-A10 infection has not been elucidated. MicroRNAs (miRNAs), implicated in the regulation of gene expression in a posttranscriptional manner, play a vital role in the pathogenesis of various central nervous systems (CNS) diseases; thereby they are served as diagnostic biomarkers and are emerging as novel therapeutic targets for CNS injuries. To gain insights in the CV-A10-induced regulation of host miRNA-processing machinery, we employed high-throughput sequencing to identify differentially expressed miRNAs in CV-A10-infected HUVEC cells and further analyzed the potential functions of these miRNAs during CV-A10 infection. The results showed that CV-A10 infection could elicit 189 and 302 significantly differentially expressed miRNAs in HUVEC cells at 24 hpi and 72 hpi, respectively, as compared with the uninfected control.
2023-07-26 | GSE236620 | GEO
Project description:Alcelaphine gammaherpesvirus 1 (AlHV-1) is a member of the Gammaherpesvirinae subfamily and establishes asymptomatic latent infection in its natural host species, the wildebeest. Cross-species transmission to various ruminant species including cattle can occur, resulting in the induction of malignant catarrhal fever (MCF), a deadly peripheral T cell lymphoproliferative disease. Here, we experimentally infected calves to confirm that AlHV-1 latency-associated gene expression is essential for persistent infection of CD8+ T cells and MCF development. Then, deep sequencing of the T cell receptor repertoire revealed an oligoclonal expansion of peripheral CD8+ T cells during bovine MCF, associated with transcriptomic and epigenetic changes identified by (sc)RNA-seq and ATAC-seq analyses which indicated a mixed effector/memory and exhaustion phenotype of infected cells in vivo. Analysis of the viral genome transcription identified viral genomic regions being expressed in infected CD8+ T cells, such as the region predicted to encode the gene A10. A10 encodes a transmembrane signaling protein displaying multiple tyrosine residues, with predicted ITAM and SH3 motifs. We could demonstrate that impaired expression of A10 did not affect AlHV-1 replication in vitro but rendered AlHV-1 unable to induce MCF in the rabbit experimental model, and we showed that A10 is phosphorylated in T lymphocytes in vitro and affects T cell signaling. Finally, while AlHV-1 viruses expressing mutated forms of A10 devoid of ITAM and/or SH3 motifs could induce MCF, an A10 knock-in viral mutant unable to phosphorylate tyrosine residues resulted in the absence of MCF development. Overall, we identified AlHV-1-induced phenotypic changes in CD8+ T cells during MCF and demonstrated that A10 expression in infected CD8+ T lymphocytes results in the dysregulation of T cell signaling and MCF.
2024-05-01 | GSE253727 | GEO
Project description:Ammonia-oxidizing Archaea enrichment culture from freshwater sediment - Nitrosarchaeum sp. BO1
| PRJNA1014936 | ENA
Project description:We found that both A9 (amiR-RH6) and A10 (amiR-RH7)-AAVs significantly decrease osteogenic differentiation of FOP-iPSCs. We also observed that A9 and A10-AAVs treatment changed the ratio of R206H mutant to wildtype of ACVR1 in FOP-iPSCs. To identify off-target effect of A9 or A10-AAVs, we compared RNA expression of FOP-iPSCs treated with control, A9, or A10-AAVs.
2022-09-20 | GSE213579 | GEO
Project description:Although a considerable number of reports indicate an involvement of the Hox-A10 gene in the molecular control of hematopoiesis, the conclusions of such studies are quite controversial since they support, in some cases, a role in the stimulation of stem cell self-renewal and myeloid progenitor expansion while, in others, implicate this transcription factor in the induction of monocyte - macrophage differentiation. To clarify this issue we analyzed the biological effects and the transcriptome changes determined in human primary CD34+ hematopoietic progenitors by retroviral transduction of a full length Hox-A10 cDNA. The results obtained clearly indicated that this homeogene is an inducer of monocyte differentiation, at least partly acting through the up-regulation of MafB gene, recently identified as master regulator of such maturation pathway. By using a combined approach based on computational analysis, EMSA experiments and luciferase assays, we were able to demonstrate the presence of a Hox-A10 binding site in the promoter region of the MafB gene, which suggested the likely molecular mechanism underlying the observed effect. Interestingly, stimulation of the same cells with the Vitamin D3 monocyte differentiation inducer resulted in a clear increase of Hox-A10 and MafB transcripts, indicating the existence of a precise transactivation cascade involving VDR, Hox-A10 and MafB transcription factors. Altogether these data allow to conclude that the Vitamin D3 / Hox-A10 pathway supports MafB function during the induction of monocyte differentiation. Experiment Overall Design: RNA pools (100 ng) of LXIDN and LHoxA10IDN transduced CD34+ cells, obtained from three independent experiments, were converted in labelled cRNA according with the âTwo cycleâ protocol advised by Affymetrix. cRNA has been used to hybridise Affymetrix HG-U133A GeneChip arrays. Images obtained by scanning chips of LXIDN and LHoxA10IDN transduced CD34+ cells were processed using the GeneChip Operating Software. Microarray analysis of Hox-A10 transduced CD34+ cells provided a substantial contribute for a better comprehension of the biological effects driven by this transcription factor in human primary hematopoietic stem / progenitor cells. Results of this analysis confirmed the stimulatory effect exerted by Hox-A10 on monocytopoiesis, disclosing an up-regulated expression of transcription factors and differentiation markers (CD antigens, granule proteins, cytokines / chemokines) that are typically associated with this maturation lineage. In addition, they also evidenced a decreased expression of genes related to erythroid and granulocyte differentiation programs. This last effect was also confirmed by cytochemical and morphological evaluation of Hox-A10 transduced CD34+ cells.
2008-10-21 | E-GEOD-12396 | biostudies-arrayexpress