Ontology highlight
ABSTRACT:
PROVIDER: PRJNA955230 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Candida albicans is exposed to a different host environment during oropharyngeal candidiasis (OPC) compared to hematogenously disseminated candidiasis. Thus, different virulence factors may be active during these two types of infection. However,little is known about the C. albicans genes that are required for the initiation and maintenance of OPC. To identify potential virulence factors relevant to this disease, we determined the transcriptional response of C. albicans to oral epithelial cells in vitro. Keywords: cell interaction Two different Candida albicans strains, CAI4-URA and a clinical isolate 7392, were used to identify the transcriptional response of C. albicans to oral epithelial cells. The strains were incubated with either the FaDu oral epithelial cell line or bare plastic for 45, 90, and 180 min. C. albicans RNA was extracted and the transcriptional profile of these organisms was analyzed using the C. albicans oligonucleotide microarray. The transcriptional response to Fadu cells was compared to that to bare plastic as a control condition. Each time point contains six biological replicates, three of which are from each C. albicans strain.
2010-06-24 | E-GEOD-5340 | biostudies-arrayexpress
Project description:Candida albicans is exposed to a different host environment during oropharyngeal candidiasis (OPC) compared to hematogenously disseminated candidiasis. Thus, different virulence factors may be active during these two types of infection. However,little is known about the C. albicans genes that are required for the initiation and maintenance of OPC. To identify potential virulence factors relevant to this disease, we determined the transcriptional response of C. albicans to oral epithelial cells in vitro. Keywords: cell interaction
2008-12-01 | GSE5340 | GEO
Project description:The objective of this study was to understand the impact of autoimmune regulator (AIRE) on immunity against oral Candida albicans infection. Previous work indicated that autoantibodies against IL-17 and IL-22 may contribute to host susceptibility; however, there is not a 100% correlation between autoantibodies and mucosal candidiasis in autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) patients, indicating that other pathways may be affected. Using a mouse model that very closely mimics what is seen in APECED patients, oral epithelial cells were sorted and RNA extracted from them to perform RNA-seq analysis to determine what other pathways may be involved. These data show that the type II interferon pathway is highly upregulated in Aire-deficient mice, while the IL-17R pathway is intact.
2021-08-11 | GSE133603 | GEO
Project description:The effects of Candida albicans on the metastatic activity of oral squamous cell carcinoma was observed in vitro and in vivo. In the in vitro experimental setup HO-1-N-1 and HSC-2 human oral squamous cell carcinoma cell lines were treated with zymosan, heat-killed Candida albicans, heat-killed C. parapsilosis, live C. albicans and live C. parapsilosis. Whole transcriptomics was performed of the human tumor cells. In the in vivo experiment human HSC-2 tumor cells were injected to the tongue of mice. Whole transcriptomic analysis was performed of the human HSC-2 derived tumor cells comparing control tumor and oral candidiasis treated tumor.
2021-12-08 | GSE169278 | GEO
Project description:Constitutive activation of the nuclear factor-kappa B (NF-kB) pathway is a hallmark of the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL). Recurrent mutations of NF-kB regulators that cause constitutive activity of this oncogenic pathway have been identified. However, it remains unclear how specific target genes are regulated. We identified the IkB-like protein NFKBIZ that binds NF-kB subunits and enhances transactivation of some NF-kB target genes while repressing others, to be upregulated in ACB compared to GCB DLBCL primary patient samples (p=5.1 x 10^-37). Knockdown of NFKBIZ by RNA interference was toxic to ABC but not GCB DLBCL cell lines. Gene expression profiling following NFKBIZ knockdown significantly downregulated a large number of NF-kB target genes, suggesting a central role in regulating NF-kB signaling. To further investigate the molecular mechanisms of how NFKBIZ mediates NF-kB signaling in ABC DLBCL, we performed immunoprecipitations and detected an interaction of NFKBIZ with both p50 and p52 NF-kB subunits, indicating that both the canonical and non-canonical NF-kB pathways are regulated by NFKBIZ. Collectively, our data imply that NFKBIZ is required for NF-kB signaling in ABC DLBCL and thus might represent a promising molecular target for future therapies. The complete dataset is comprised of three experiments with the male HBL-1 ABC DLBCL cell line: a) 8 paired GEP measurements after NFKBIZ inhibition by shRNA, b) 6 paired GEP measurements after applying the MLN inhibitor and c) 4 two-color measurements after applying a MALT inhibitor. This dataset includes 8 paired GEP measurements after NFKBIZ inhibition by shRNA.
2013-07-22 | E-GEOD-46971 | biostudies-arrayexpress
Project description:Constitutive activation of the nuclear factor-kappa B (NF-kB) pathway is a hallmark of the activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL). Recurrent mutations of NF-kB regulators that cause constitutive activity of this oncogenic pathway have been identified. However, it remains unclear how specific target genes are regulated. We identified the IkB-like protein NFKBIZ that binds NF-kB subunits and enhances transactivation of some NF-kB target genes while repressing others, to be upregulated in ACB compared to GCB DLBCL primary patient samples (p=5.1 x 10^-37). Knockdown of NFKBIZ by RNA interference was toxic to ABC but not GCB DLBCL cell lines. Gene expression profiling following NFKBIZ knockdown significantly downregulated a large number of NF-kB target genes, suggesting a central role in regulating NF-kB signaling. To further investigate the molecular mechanisms of how NFKBIZ mediates NF-kB signaling in ABC DLBCL, we performed immunoprecipitations and detected an interaction of NFKBIZ with both p50 and p52 NF-kB subunits, indicating that both the canonical and non-canonical NF-kB pathways are regulated by NFKBIZ. Collectively, our data imply that NFKBIZ is required for NF-kB signaling in ABC DLBCL and thus might represent a promising molecular target for future therapies. The complete dataset is comprised of three experiments with the male HBL-1 ABC DLBCL cell line: a) 8 paired GEP measurements after NFKBIZ inhibition by shRNA, b) 6 paired GEP measurements after applying the MLN inhibitor and c) 4 two-color measurements after applying a MALT inhibitor. This dataset includes 6 paired GEP measurements after applying the MLN inhibitor.
2013-07-22 | E-GEOD-46972 | biostudies-arrayexpress
Project description:Regulation of lineage biases in hematopoietic stem and progenitor cells (HSPCs) is pivotal for balanced hematopoietic output. However, little is known about the mechanism behind lineage choice in HSPCs. Here, we show that mRNA decay factors Regnase-1 (Zc3h12a) and Regnase-3 (Zc3h12c) are critical for induction of myeloid lineage priming, restricting lymphoid differentiation in HSPCs. Regnase-1- and Regnase-3-mediated control of mRNA encoding Nfkbiz, a transcriptional and epigenetic regulator, was essential for balancing lymphoid/myeloid lineage output in HSPCs in vivo. Furthermore, single cell-assay for transposase-accessible chromatin sequencing (scATAC-seq) analysis revealed that Regnase-1 and Regnase-3 control the epigenetic landscape on myeloid-related gene loci in hematopoietic stem cells (HSCs) via Nfkbiz. Consistently, an antisense oligonucleotide designed to inhibit Regnase-1- and Regnase-3-mediated Nfkbiz mRNA degradation primed HSCs toward myeloid lineages by enhancing Nfkbiz expression. Collectively, the collaboration between post-transcriptional control and chromatin remodeling by the Regnase-1/Regnase-3-Nfkbiz axis governs lineage priming, instructing HSC lineage specification.
2023-07-31 | GSE229065 | GEO