Agents which upregulate CD55 [decay accelerating factor (DAF)] expression [Array]
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ABSTRACT:
PROVIDER: PRJNA1073479 | ENA |
REPOSITORIES: ENA
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Project description:(Submitter supplied) Identification of transcription factors (TFs) which upregulate human CD55 expression. CD55 was originally described as a cellular complement regulator that protects self-cells from autologous complement attack. It is now known as cellular regulator which controls many functions of cells, as examples T cell commitment to T effector cells vs Foxp3+ T regulatory cells, B2 cell Ab production, and receptor tyrosine kinase (RTK) growth factor receptor function. Overlap of the arrays identified the immunosuppressive TF Kruppel Like Factor 4 (KLF4). The current study shows that CD55 functions jointly with KLF4.
2024-02-12 | GSE255080 | GEO
Project description:Mus musculus Cd55, CD55 molecule, decay accelerating factor for complement [Source:MGI Symbol;Acc:MGI:104850], is differentially expressed in 151 experiment(s);
| ENSMUSG00000026399 | ExpressionAtlas
Project description:Mus musculus Cd55, CD55 molecule, decay accelerating factor for complement [Source:MGI Symbol;Acc:MGI:104850], is expressed in 37 baseline experiment(s);
| ENSMUSG00000026399 | ExpressionAtlas
Project description:Germinal centers (GCs) support diversification and affinity maturation of antibody repertoires through iterative cycles of T-cell-dependent positive selection, B cell clonal expansion and antigen-receptor hypermutation. Positive selection is critical for efficient affinity maturation and depends on only partially understood signaling processes. We show that BCL6-dependent physiological repression of decay accelerating factor (DAF/CD55) on GC B cells is critical for effective positive selection and affinity maturation during GC responses. Absence of DAF on GC B cells lifts restraint on local complement activation, yielding autocrine C3a/C5a-receptor signaling that is indispensable for CD40-dependent mTOR pathway activation during positive selection. Genetic disruption of this pathway causes premature GC collapse and impairs affinity maturation. These results identify previously undiscerned targets to therapeutically manipulate protective and potentially injurious humoral immune responses.
2021-03-22 | GSE148570 | GEO
Project description:Molecular cloning of mouse decay accelerating factor (DAF; CD55) predicted two forms of the molecule, one transmembrane (TM) and the other glycosylphosphatidylinositol (GPI)-anchored; these are encoded by separate genes termed Daf-GPI and Daf-TM. In the present study several additional isoforms of mouse DAF, generated by alternative splicing from these genes, are described. Northern-blot analysis of RNA and reverse transcriptase-PCR from various tissues indicated that spleen and testis expressed high levels of DAF, which comprised several species. These species were cloned and sequence analysis revealed various novel forms in addition to those previously reported. Two novel forms were derived from the Daf-TM gene but the transmembrane sequence defined previously was replaced by a unique GPI-anchor addition sequence; one clone also had part of the serine/threonine/proline (STP) region deleted. A third clone, encoding a transmembrane protein, was also derived from this gene but the entire STP region was deleted. A fourth clone, derived from the Daf-GPI gene, contained a novel C-terminal sequence, suggestive of a secreted form of the protein. Two DAF cDNAs (TM and GPI-anchored) were stably expressed in Chinese hamster ovary cells. When these cells were attacked with mouse or rat complement and analysed for C3b deposition, DAF-transfected cells had greatly reduced C3b deposition compared with controls. Transfection with DAF also conferred protection from complement in a cell-lysis assay, and a soluble, recombinant form of mouse DAF inhibited complement in a haemolytic assay.
| S-EPMC1220423 | biostudies-other
Project description:BackgroundType 1 diabetes (T1D) is a common autoimmune disease resulting from T-cell mediated destruction of pancreatic beta cells. Decay accelerating factor (DAF, CD55), a glycosylphosphatidylinositol-anchored membrane protein, is a candidate for autoimmune disease susceptibility based on its role in restricting complement activation and evidence that DAF expression modulates the phenotype of mice models for autoimmune disease. In this study, we adopt a linkage disequilibrium (LD) mapping approach to test for an association between the DAF gene and T1D.ResultsInitially, we used HapMap II genotype data to examine LD across the DAF region. Additional resequencing was required, identifying 16 novel polymorphisms. Combining both datasets, a LD mapping approach was adopted to test for association with T1D. Seven tag SNPs were selected and genotyped in case-control (3,523 cases and 3,817 controls) and family (725 families) collections.ConclusionWe obtained no evidence of association between T1D and the DAF region in two independent collections. In addition, we assessed the impact of using only HapMap II genotypes for the selection of tag SNPs and, based on this study, found that HapMap II genotypes may require additional SNP discovery for comprehensive LD mapping of some genes in common disease.
| S-EPMC1479364 | biostudies-literature
Project description:To exmine the role of nonsense-mediated mRNA decay process in the longevity regulation of daf-2 mutants, we sequenced transcriptomes from day 1 adult Caenorhabditis elegans: Bristol N2 (wild-type), and smg-2(qd101), daf-2(e1370) and smg-2(qd101); daf-2(e1370) mutants.
2017-03-17 | GSE94077 | GEO
Project description:Germinal centers (GCs) are structures in secondary lymphoid organs, essential for an efficient humoral immune response. Complement interaction with B cells facilitates B cell activation, but little is known about the role of complement regulators during B cell activation and differentiation. By flow cytometric analysis, we could show that the majority of human GC B cells had decreased expression of the negative complement regulator Decay Accelerating Factor (DAF). Transcriptomic analysis revealed that DAFlo GC B cells upregulated genes associated with gene editing and proliferation, whereas DAFhi GC B cells had increased expression of genes involved in cell differentiation. We could confirm that DAFhi GC B cells expressed the transcription factor Blimp1 on protein level, which indicates that DAFhi GC B cells may be early plasmablasts/plasma cells. Then, we assessed the expression of the complement regulator CD59, which inhibits the membrane attack complex that lyses cells. We found that the expression was low in naïve and memory B cells, but increased in GC and plasmablasts/plasma cells. This suggests that DAFlo GC B cells may be primed for phagocytosis rather than lysis. By cell sorting, we could show that DAFlo GC B cells were phagocytosed to a greater extent than DAFhi GC B cells, both in presence and absence of complement. Stimulation of the B cell receptor on circulating B cells induced DAFlo cells. Finally, we also identified specific downregulation of DAF during early B cell development in the human bone marrow. As a conclusion, we suggest that complement regulators serve specific functions at stages of B cell selection.
2020-12-31 | GSE153741 | GEO
Project description:We previously reported that nitric oxide (NO) reduces the rate of bacteremia and maternal mortality in pregnant rats with uterine infection by Escherichia coli expressing the Dr Fimbria (Dr(+) ). The epithelial invasion of Dr(+) E. coli is dependent on the expression level of its cellular receptor decay accelerating factor (DAF). NO reduces the rate of bacteremia by downregulating the expression of DAF. In this study, we elucidated the role of transcription factor Sp1 and RNA binding protein HuR in the downregulation of human DAF by NO. We generated a series of deletion mutant constructs of DAF gene 5'-untranslated region and mapped the NO-response region upstream to the core promoter region of the DAF gene. One of the several Sp1 binding sites in the DAF 5'-untranslated region was located within the NO-response region. The binding of Sp1 to this site was inhibited by NO. Furthermore, NO also promoted the degradation of DAF mRNA. The 3'-untranslated region of DAF harbors an AU-rich element and this element destabilized the mRNA transcript. NO promoted the rapid degradation of DAF mRNA by inhibiting the binding of mRNA stabilizing protein HuR to this AU-rich region. The inhibition of binding of HuR to the AU-rich region was due to the S-nitrosylation of one or more cysteine residues by NO. Thus, these data reveal the molecular mediators of transcriptional and post-transcriptional regulation of DAF by NO with implications in pathophysiology related to DAF.
| S-EPMC3558599 | biostudies-literature
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare the genes expression difference at transcriptome level; Methods: Total RNA was extracted from whole cells with the mirVana miRNA Isolation Kit according to the manufacturer’s protocol. RNA quality and integrity were evaluated with an Agilent 2100 Bioanalyzer. Samples with an RNA integrity number (RIN) ≥ 7 were considered to be of high quality and were processed further and subjected to subsequent analysis. Total RNA-seq libraries were generated using 4 μg of total RNA, which was analyzed using the TruSeq Stranded mRNA LTSample Prep Kit. These libraries were then sequenced using the Illumina sequencing platform (HiSeqTM 2500 or Illumina HiSeq X Ten), and 125-bp/150-bp paired-end reads were generated. Results: The raw reads containing adaptors and the low-quality reads from the raw data were removed using Trimmomatic to obtain clean reads. Transcriptome sequencing was conducted by OE Biotech Co., Ltd. (Shanghai, China), and clean reads were provided. The clean reads were mapped to the hg38 reference genome using hisat2 (version 2.1.0). The output BAM files were converted to SAM files using SAMtools 1.9. The final TPM values were obtained using Stringtie 1.3.5. Conclusions: To understand the mechanistic basis of GPI biosynthesis upregulation by the CD55 precursor, we performed RNA- sequencing (RNA-seq) of samples of parental PIGS-HRD1-DKO, PIGS-HRD1-CD55-TKO, and PIGS-HRD1-CD55-TKO stably overexpressed HA-CD55 stably overexpressing cells. Total RNA was extracted and analyzed. The expression profile of GPI biosynthesis -related genes was not significantly affected by CD55.
2021-09-29 | GSE184822 | GEO