Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Agents which upregulate CD55 [decay accelerating factor (DAF)] expression [Array]

ABSTRACT: Agents which upregulate CD55 [decay accelerating factor (DAF)] expression [Array]

PROVIDER: PRJNA1073479 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Agents which upregulate CD55 [decay accelerating factor (DAF)] expression [Array]

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

Transcriptional profiling of mouse germinal center B cells (B220+, GL7+, CD95+) isolated from GC-specific (Cg1-Cre) DAF-TM transgenic or control mice

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

Molecular and functional analysis of mouse decay accelerating factor (CD55).

Project description: Not available

| S-EPMC1220423 | biostudies-other

Discovery, linkage disequilibrium and association analyses of polymorphisms of the immune complement inhibitor, decay-accelerating factor gene (DAF/CD55) in type 1 diabetes.

Project description: Not available

| S-EPMC1479364 | biostudies-literature

Analysis of nonsense-mediated mRNA decay in daf-2 mutants

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

Regulation of Decay Accelerating Factor primes human germinal center B cells for phagocytosis

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

Role of transcription factor Sp1 and RNA binding protein HuR in the downregulation of Dr+ Escherichia coli receptor protein decay accelerating factor (DAF or CD55) by nitric oxide.

Project description: Not available

| S-EPMC3558599 | biostudies-literature

Next Generation Sequencing Facilitates Quantitative Analysis of PIGS-KO, PIGS-HRD1-DKO, PIGS-HRD1-CD55-TKO, and PIGS-HRD1-CD55-TKO+HA-CD55 Transcriptomes

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

N2, daf-1(m40), and daf-1(m40);daf-3(mgDf90) adult, gravid hermaphrodites

Project description:total RNA from N2, daf-1(m40), and daf-1(m40);daf-3(mgDf90) adult, gravid hermaphrodites were extracted and sequenced.

2020-05-28 | GSE131997 | GEO

Complement-regulated Homeostatic Proliferation Controls Memory B Cell Longevity and Repertoire Composition

Project description:Memory B cell (Bmem) survival is essential for guarding against reinfection, yet processes ensuring their longevity remain unclear. As decay-accelerating factor (DAF, CD55), a negative regulator of complement activation, is requisitely downregulated on germinal center B cells and is re-expressed on Bmem, we investigated the effects of deleting DAF on murine (B1-8hi) Bmem in competitive settings. Kinetic analysis showed a progressive reduction in DAF-/- Bmem numbers over six weeks, without affecting Bmem production, pool size, or their ability to respond to rechallenge. Following transfer into unimmunized hosts, wild-type Bmem proliferated to maintain stable Bmem pool sizes, outcompeting DAF-/- Bmem, reflecting homeostatic proliferation. Reduced proliferation and increased cell death in DAF-/- Bmem associated with transcriptional differences in metabolism and migration pathways. Wild type Bmem proliferation increased in C3-/- hosts, and vaccination with a heterologous antigen, which induces local complement activation, locally inhibited bystander B1-8hi Bmem proliferation. Thus, complement-dependent regulation of Bmem homeostatic proliferation influences Bmem longevity and repertoire composition in mice.

2026-04-23 | GSE326423 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data