Affymetrix on human colon cancer cell line GP5d with siRNA against CTNNB1, MAX and MXD1 against control siRNA
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Anna Vähärautio
PROVIDER: E-MTAB-9322 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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2015-12-21 | E-GEOD-54058 | biostudies-arrayexpress
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2021-07-31 | E-MTAB-8908 | biostudies-arrayexpress
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2012-03-27 | E-GEOD-21545 | biostudies-arrayexpress
Project description:A172 cell lines were stable transfected with C19ORF63 (Human hematopoietic peptide secreted-1 - HSS1). HSS1 is a truly novel protein defining a new class of secreted factors. A172 cell line overexpressing HSS1 greatly reduced their proliferation rate compared to mock-transfected cells. Microarray analysis was used to detail gene expression underlying the anti-proliferative and anti-tumorigenic effect of HSS1 in A172 cells. Exponentially growing A172 cells at growth curve day 4 were harvested for total RNA extraction and hybridization on Affimetrix microarrays. Four groups of samples were evaluated in biological triplicates: A172 wild-type, A172 -pcDNA3.1 mock-transfected, A172-pcDNA-HSS1 clone#7 and A172-pcDNA-HSS1 clone#8. Cells were stable transfected with pcDNA3.1 empty vector or hHSS1. hHSS1-expressing cells and control cells were at confluence 40-80% when harvested. Trypan blue analysis of the number of viable cells showed a significant anti-proliferative effect in A172 cells expressing hHSS1 as compared to the control cells.
2014-12-22 | E-GEOD-61778 | biostudies-arrayexpress
Project description:U87 cell lines were stable transfected with C19ORF63 (Human hematopoietic peptide secreted-1 - HSS1). HSS1 is a truly novel protein defining a new class of secreted factors. U87 cell line overexpressing HSS1 greatly reduced their proliferation rate compared to mock-transfected cells. Microarray analysis was used to detail gene expression underlying the anti-proliferative and anti-tumorigenic effect of HSS1 in U87 cells. Exponentially growing U87 cells at growth curve day 5 were harvested for total RNA extraction and hybridization on Affimetrix microarrays. Three groups of samples were evaluated in triplicates: U87 wild-type, U87 -pcDNA3.1 mock-transfected, U87-pcDNA-HSS1. Cells were stable transfected with pcDNA3.1 empty vector or hHSS1. hHSS1-expressing cells and control cells were at confluence 40-80% when harvested. Trypan blue analysis of the number of viable cells showed a significant anti-proliferative effect in U87 cells expressing hHSS1 as compared to the control cells.
2014-12-22 | E-GEOD-61779 | biostudies-arrayexpress
Project description:Splenic Transitional Type-1 B-cells from CBA wild-type mice, X-linked immunodeficiency mice and Bruton's tyrosine kinase knock-out mice. Two replicates where run on Affymetrix 420 2.0 arrays for CBA wild-type, Xid samples and the Btk KO samples. Bruton's tyrosine kinase (Btk) is a cytoplasmic tyrosine kinase important for B-lymphocyte maturation. Mutations in Btk give rise to the primary immunodeficiency disease X-linked agammaglobulinemia (XLA) in man and X-linked immunodeficiency (Xid) in mice. Recent studies have subdivided the mouse immature, or transitional, B-cells into two distinct subsets according to their respective surface markers. Transitional type 1 (T1) and transitional type 2 (T2) cells are also located in distinct anatomic locations. Based on a limited number of markers it has previously been reported that the earliest phenotypic sign of Btk deficiency is manifested at the T2 stage in mice. Here, we report on distinct genome-wide transcriptomic signature differences found in T1 B-lymphocytes from Btk-defective compared to normal mice and demonstrate that Btk deficiency is visible already at this stage. 2 replicates of T1 B-cells from CBA (WT), Xid samples and the Btk KO samples
2014-01-10 | E-GEOD-53946 | biostudies-arrayexpress
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2014-12-17 | E-GEOD-61780 | biostudies-arrayexpress
Project description:To determine the effect of CyD knockdown through gapmer-mediated knockdown of PPIF gene in pathogenic functions related to wound healing
2024-04-01 | E-MTAB-13920 | biostudies-arrayexpress
Project description:Crimean-Congo hemorrhagic fever (CCHF) caused by CCHF virus (CCHFV) is one of the epidemic-prone diseases prioritized by the World Health Organisation as public health emergency with an urgent need for accelerated research. The trajectory of host response against CCHFV is multifarious and remains unknown. Here, we reported the temporal spectrum of pathogenesis following the CCHFV infection using genome-wide blood transcriptomics analysis followed by advanced systems biology analysis, temporal immune-pathogenic alterations, and context-specific progressive and postinfection genome-scale metabolic models (GSMM) on samples collected during the acute (T0), early convalescent (T1), and convalescent-phase (T2). The interplay between the retinoic acid-inducible gene-I-like/nucleotide-binding oligomerization domain-like receptor and tumor necrosis factor signaling governed the trajectory of antiviral immune responses. The rearrangement of intracellular metabolic fluxes toward the amino acid metabolism and metabolic shift toward oxidative phosphorylation and fatty acid oxidation during acute CCHFV infection determine the pathogenicity. The upregulation of the tricarboxylic acid cycle during CCHFV infection, compared to the noninfected healthy control and between the severity groups, indicated an increased energy demand and cellular stress. The upregulation of glycolysis and pyruvate metabolism potentiated energy generation through alternative pathways associated with the severity of the infection. The downregulation of metabolic processes at the convalescent phase identified by blood cell transcriptomics and single-cell type proteomics of five immune cells (CD4+ and CD8+ T cells, CD14+ monocytes, B cells, and NK cells) potentially leads to metabolic rewiring through the recovery due to hyperactivity during the acute phase leading to post-viral fatigue syndrome.
2023-10-11 | PXD038929 | Pride
Project description:Background: Ameloblast differentiation is the most critical stepwise process in amelogenesis and controlled by a precisely molecules synergistically. To better understand the molecular events defining cell differentiation between preameloblasts and secretory ameloblasts during amelogenesis, a more precise identification of molecules and signaling networks would shed light on the mechanisms governing enamel formation and help lay a foundation for enamel regeneration. Results: Gene expression profiles of human preameloblast and secretory ameloblast cells were obtained using human genome microarrays. From a total of 28,869 analyzed transcripts, 923 differentially expressed genes (DEGs) with FDR<0.01 and Fold-change > 2 were obtained. Among them, more than twice DEGs were found enriched in PAB (n = 647) compared with SAB (n = 276). Notably, 38 genes were identified significantly differentially expressed between PAB and SAB (Fold Change > 8). Comparison of transcriptional profiles of PAB and SAB together with KEGG pathway analysis revealed genes enrichment in PAB were chiefly involved in cell cycle control, DNA damage repair and apoptosis, while genes related to cell adhesion and extracellular matrix had elevated expression level in SAB. Two co-expression modules were further identified significantly associated with the ameloblast differentiation process by weighted gene co-expression network analysis (WGCNA).These gene networks seem to contribute to cell adhesion, tissue development, cell signaling and division. Furthermore, the co-expression associations of RunX2 and BMP8A were also observed in these modules. Conclusions: In this study, we uncovered that the differentiation from PAB to SAB may rely on a highly regulated network of interactions between conserved signal transduction pathways, including members of BMP/TGF-β, Notch, MAPK pathways to coordinate all aspects of ameloblast in intracellular processes and their social contexts. Specifically, expression of genes associated with cell cycle control, DNA damage repair, and apoptosis pathways regulates pre-ameloblast maturation during tooth development. And the SAB cells are regulated by several signaling pathways controlling enamel matrix proteins secretion and cell adhesion, which are critical for enamel formation and cell-cell interactions. Apart from showing the transcriptional patterns of PAB and SAB, the application of bioinformatic analysis also explored the potential key genes and gene-associations in ameloblast differentiation. These findings will aid in the design of new strategies to promote ameloblast functional differentiation in the regeneration and tissue engineering of teeth. Human tooth buds (18-22 weeks) were obtained from fetal cadaver tissue within 3 hours after legal abortion. Teeth were dissected from the mandibles under a laminar flow hood, embedded in OCT compound, and cryosectioned at 10-μm thickness. These sections were used for laser capture microdissection (LCM). In total of 3 pre-ameloblasts and 3 secretory ameloblasts pooled samples were used for RNA extraction and hybridization on Affymetrix microarray.
2014-10-01 | E-GEOD-59214 | biostudies-arrayexpress