E-GEOD-43075
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA184347
PROVIDER: E-GEOD-43075 | ExpressionAtlas | 2015-07-08
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-43075-analysis-methods.tsv | Tabular | |||
| E-GEOD-43075-atlasExperimentSummary.Rdata | Rdata | |||
| E-GEOD-43075-configuration.xml | Xml | |||
| E-GEOD-43075-percentile-ranks.tsv | Tabular | |||
| E-GEOD-43075.condensed-sdrf.tsv | Tabular |
Items per page: 5 1 - 5 of 71 |
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Project description:Inhibitor of NFκB ζ (IκBζ) is a transcriptional key regulator of monocyte chemoattractant protein-1 (MCP-1/CCL2)
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Project description:Monocyte chemoattractant protein 1 (MCP-1/CCL2) is critically involved in directing the migration of blood monocytes to sites of inflammation. Consequently, excessive MCP-1 secretion has been linked to many (auto)inflammatory diseases, whereas a lack of expression severely impairs immune responsiveness. We demonstrate that the atypical inhibitor of NF-κB ζ (IκBζ), a transcriptional co-activator required for the selective expression of a subset of NF-κB target genes, is a key activator of the Ccl2 gene. IκBζ-deficient macrophages exhibited impaired secretion of MCP-1 when challenged with diverse inflammatory stimuli, such as lipopolysaccharide or peptidoglycan. These findings were reflected at the level of Ccl2 gene expression, which was tightly coupled to the presence of IκBζ. Moreover, mechanistic insights acquired by chromatin immunoprecipitation demonstrate that IκBζ is directly recruited to the proximal promoter region of the Ccl2 gene and required for histone H3K9 trimethylation. Finally, IκBζ-deficient mice showed significantly impaired MCP-1 secretion and monocyte infiltration in an experimental model of peritonitis. Together, these findings suggest a distinguished role of IκBζ in mediating the targeted recruitment of monocytes in response to local inflammatory events. Peritoneal macrophages from Wildtype and IκBζ-Knockout mice were either stimulated with 1µg/ml LPS for 4h or left untreated (triplicates each)
2013-04-09 | E-GEOD-43075 | biostudies-arrayexpress
Project description:Monocyte chemoattractant protein 1 (MCP-1/CCL2) is critically involved in directing the migration of blood monocytes to sites of inflammation. Consequently, excessive MCP-1 secretion has been linked to many (auto)inflammatory diseases, whereas a lack of expression severely impairs immune responsiveness. We demonstrate that the atypical inhibitor of NF-κB ζ (IκBζ), a transcriptional co-activator required for the selective expression of a subset of NF-κB target genes, is a key activator of the Ccl2 gene. IκBζ-deficient macrophages exhibited impaired secretion of MCP-1 when challenged with diverse inflammatory stimuli, such as lipopolysaccharide or peptidoglycan. These findings were reflected at the level of Ccl2 gene expression, which was tightly coupled to the presence of IκBζ. Moreover, mechanistic insights acquired by chromatin immunoprecipitation demonstrate that IκBζ is directly recruited to the proximal promoter region of the Ccl2 gene and required for histone H3K9 trimethylation. Finally, IκBζ-deficient mice showed significantly impaired MCP-1 secretion and monocyte infiltration in an experimental model of peritonitis. Together, these findings suggest a distinguished role of IκBζ in mediating the targeted recruitment of monocytes in response to local inflammatory events.
2013-04-09 | GSE43075 | GEO
Project description:Transcriptional profiling reveals monocyte signature associated with JIA patient poor response to methotrexate
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Project description:Infants diagnosed of precursor B-cell acute lymphoblastic leukemia (iB-ALL) presenting MLL-AF4 chromosomal rearrangement are at high risk of disease progression into fatal outcome. This specific subtype of pediatric leukemia constitutes a tough challenge in leukemia research, given the difficulties found when trying in vivo modelling. However, the understanding of mechanisms leading to proper lymphocyte generation may become of high utility in gaining deep insight on this malignancy. As we report here, the lack of HDAC7, a key transcriptional regulator in B lymphocyte differentiation, worsens the prognosis of iB-ALL patients. In fact, MLL-AF4+ iB-ALL patients with high expression of HDAC7 display an improved survival, partially mediated by the repression of oncogenes, such as c-MYC, and chemoresistance markers, like the ASNS enzyme. Accordingly, HDAC7 drastically reduces leukemic cells proliferation in MLL-AF4+ iB-ALL through the induction of apoptosis. Moreover, RNA sequencing of HDAC7-overexpressing cells has revealed that HDAC7 alters the genomic profiling of MLL-AF4+ iB-ALL cells towards that of healthy B-cell progenitors. In summary, the findings here reported highlight the role of HDAC7 in predicting prognosis of a lethal subtype of iB-ALL and open new clinical perspectives, since MLL-AF4+ iB-ALL infants would highly benefit from therapeutic options eventually restoring HDAC7 expression.
2021-06-04 | GSE151793 | GEO
Project description:Interventions: Case series:None
Primary outcome(s): exon genes;transcriptional expression;proteome;protein phosphorylation group
Study Design: Sequential
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Project description:Iberian ham production includes both purebred (IB) and Duroc-crossbred (IBxDU) Iberian pigs, which show important differences in meat quality and production traits, such as muscle growth and fatness. This experiment was conducted to investigate gene expression differences, transcriptional regulation and genetic polymorphisms that could be associated with the observed phenotypic differences between IB and IBxDU pigs. Nine IB and 10 IBxDU pigs were slaughtered at birth. Morphometric measures and blood samples were obtained and samples from Biceps femoris muscle were employed for compositional and transcriptome analysis by RNA-Seq technology. Phenotypic differences were evident at this early age, including greater body size and weight in IBxDU and greater Biceps femoris intramuscular fat and plasma cholesterol content in IB newborns. We detected 150 differentially expressed genes between IB and IBxDU neonates (p < 0.01 and Fold-Change > 1. 5). Several were related to adipose and muscle tissues development (DLK1, FGF21 or UBC). The functional interpretation of the transcriptomic differences revealed enrichment of functions and pathways related to lipid metabolism in IB and to cellular and muscle growth in IBxDU. Protein catabolism, cholesterol biosynthesis and immune system were functions enriched in both genotypes. We identified transcription factors potentially affecting the observed gene expression differences. Some of them have known functions on adipogenesis (CEBPA, EGRs), lipid metabolism (PPARGC1B) and myogenesis (FOXOs, MEF2D, MYOD1), which suggest a key role in the meat quality differences existing between IB and IBxDU hams. We also identified several polymorphisms showing differential segregation between IB and IBxDU pigs. Among them, non-synonymous variants were detected in several transcription factors as PPARGC1B gene, which could be associated to altered gene function. Taken together, these results provide information about candidate genes, metabolic pathways and genetic polymorphisms potentially involved in phenotypic differences between IB and IBxDU associated to meat quality and production traits.
2016-09-25 | GSE73566 | GEO
Project description:Gene-level transcriptome analysis of monocyte mRNA derived from mice that are genetically deficient of the Ccl2 gene or Ccr2 gene The CCL2/CCR2 chemokine axis is critical in monocytes mobilization and innate immunity. Although mice deficient in either gene manifest similar phenotype, such as reduced atherosclerosis, some biologic processes are disrupted in starkly different ways in these mice. We found in a Her2/neu driven mammary carcinoma model, the absence of Ccl2 inhibits tumor growth and prolongs survival, while genetic deletion of Ccr2 has the opposite effect. One of the postulated mechanisms is that Ccl2 and Ccr2 affect monocyte development in different manners. This experiment was designed to compare the whole transcriptome of monocytes that are deficient in either Ccl2 or Ccr2, with the hypothesis that differential development of these monocytes will manifest as differential gene expression profiles.
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Project description:The protein kinase MLTK Is a key regulator for chondrogenesis.
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Project description:Purpose: Intermuscular bones (IBs) are hard spicules, mainly existing in the myosepta of recent vertebrates. This evolutionary trait has puzzled biologists and consumers, and the molecular basis of IB development remains unclear. The goals of this study are to acquire characteristic single-cell maps of gene expression landscapes and lineages and to elucidate the differentiation trajectory of cell clusters related to IB formation and obtain the key regulated gene of IB formation. Methods: The scRNA-seq profiles of 60 dpf wild-type zebrafish and 60 dpf runx2b-/- zebrafish were generated, using the 10X Genomics Chromium system. The bulk RNA-seq profiles of 60 dpf wild-type zebrafish and 60 dpf runx2b-/- zebrafish were generated, using mirVana™ miRNA ISOlation Kit. The scRNA-seq data were filted and clsutered by the Seurat package. The cell differentiation trajectorie was constructed, using Monocle analysis. Runx2b knockdown was preformed by RNA interference and runx2b was inducted by neuropeptide substance P. qRT–PCR validation was performed using SYBR Green assays. The mutant zebrafish lines were constructed, using cripsr cas9 technology.The Phenotypic observation was perfomed by Hematoxylin and Eosin (HE), Alizarin red, masson trichrome staining and mico-CT. The nutritent content was also obtained including fatty acid content and anio acid content. Results: we reveal that teleost fish IBs originate from tendons in the skeletal muscle and that the differentiation trajectory from tendon progenitors and defined runx2b as the key rugulated gene of IB formaiton, using cripsr cas9 technology. Conclusions: This study is the first to reveal that teleost fish IBs originate from tendons in the skeletal muscle and that the differentiation trajectory from tendon progenitors to the osteoblast lineage is key for IB formation. Large-scale gene function analysis using CRISPR-Cas9 identified the decisive role of runx2b in IB formation. The loss of runx2b significantly restricted osteoblast differentiation and inhibited IB formation, which potentially provides a basis for breeding strains of fish without IBs to improve the safe consumption and economic value of many aquaculture species and in this way, boost the proportion of fish for the supply of animal protein worldwide (Fig. 6). For this reason, we needed to verify that the content of fatty acid in the runx2b−/− mutant was higher than that in runx2b+/+ fish, as well as the expression of key genes related to IBs in the runx2b−/− and runx2b+/+ strains obtained by scRNA-seq data. This study also provides materials and directions for further study to clarify the specific regulatory mechanism of IB formation and will help to discover more specific genetic resources that can be used for IB trait improvement in fish.
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