Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Adhesion GPCR CD97 promotes spleen dendritic cell retention and function through sensing of CD55-expressing red blood cells

ABSTRACT: Adhesion GPCR CD97 promotes spleen dendritic cell retention and function through sensing of CD55-expressing red blood cells

PROVIDER: PRJNA780483 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16947313.fastq.gz	Fastqsanger.gz
	SRR16947314.fastq.gz	Fastqsanger.gz
	SRR16947315.fastq.gz	Fastqsanger.gz
	SRR16947316.fastq.gz	Fastqsanger.gz
	SRR16947317.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 15

Similar Datasets

Adhesion GPCR CD97 promotes spleen dendritic cell retention and function through sensing of CD55-expressing red blood cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-23 | GSE188835 | GEO

CD97 is a Critical Regulator of Acute Myeloid Leukemia Stem Cell Function

Project description:Despite significant efforts to improve therapies for acute myeloid leukemia (AML), clinical outcomes remain poor. Understanding the mechanisms that regulate the development and maintenance of leukemic stem cells (LSC) is important to reveal new therapeutic opportunities. We have identified CD97, a member of the adhesion class of G-protein coupled receptors (GPCRs), as a frequently upregulated antigen of AML blasts that is a critical regulator of blast function. High levels of CD97 correlate with poor prognosis, and silencing of CD97 reduces disease aggressiveness in vivo. In order to analyze the functional pathways associated with CD97 expression, we generated RNA-sequence data from scrambled shRNA transfected (s-shRNA) and CD97 KD human AML cell line HL60, as well as from MLL-AF9 (MA9) transduced GMPs isolated from CD97-/- and WT mice. These phenotypes are due to CD97’s function to promote proliferation, survival, and the maintenance of the undifferentiated state in leukemic blasts. Collectively, our data credential CD97 as a promising therapeutic target on LSCs in AML.

2019-07-30 | GSE135028 | GEO

RNA-sequencing of wild-type, CD97- and Gα13-deficient splenic cDC2s

Project description:We analyzed the transcriptome differences of wild-type, CD97- and Gα13-deficient (Adgre5-/- and CD11c-cre x Gna13fl/fl) type-2 conventional dendritic cells (cDC2s) in spleen. Three technical repeats of ~10^5 cells per sample from each of one mouse were included. Compared to wild-type cDC2s, CD97- and Gα13-deficient cDC2s differentially expressed many genes, but CD97- and Gα13-deficient cDC2s were almost the same. GSEA showed that Mrtf-a dependent genes were upregulated in CD97- and Gα13-deficient cDC2s, which code for cytoskeleton proteins. These data support that CD97-Gα13 signaling regulates splenic cDC2 motility by the actin cytoskeleton.

2022-03-23 | GSE188828 | GEO

Data for Alternative Splicing of Adhesion-GPCR Latrophilin-3 Controls Synapse Formation

Project description:Data for Alternative Splicing of Adhesion-GPCR Latrophilin-3 Controls Synapse Formation

| PRJNA1005253 | ENA

Adhesion GPCR ADGRE2 maintains proteostasis to promote progression in acute myeloid leukemia

Project description:Adhesion GPCR ADGRE2 maintains proteostasis to promote progression in acute myeloid leukemia

| PRJNA1087687 | ENA

Next Generation Sequencing from control and CD97 knockdown of glioblastoma stem cells

Project description:Glioblastoma (GBM) stem cells (GSCs) are largely associated with a poor prognosis of GBM. Although the importance of identifying and validating molecular markers in GBM has been emphasized, single markers covering all GSCs are lacking. Through in vitro antibody screening, in this study, we demonstrated that CD97 identifies GSCs as a novel surface marker. Compared to conventional well-known GSC markers, such as CD133, CD44 and CD15, only CD97 was notably detected in all tested patient-derived GSCs. GBM patients expressing high levels of CD97 experienced worse clinical outcomes, and were predictive of poor overall survival in the public database. CD97 is required for GSC proliferation and self-renewal and was shown to reduce mouse survival with aggressive tumor progression in an orthotopic xenograft model. A comparative transcriptomic analysis revealed that CD97 triggers mTORC2 signaling through Akt (S473) phosphorylation, enhancing the expression of downstream genes, including ARHGAP1, BZW1, and BZW2. Moreover, inhibition of mTORC2 signaling with the pharmacological inhibitor JR-AP2-011 suppressed GSC proliferation, self-renewal, and downstream gene expression. Furthermore, sorting of CD97-enriched cells from patient-derived GSCs revealed that CD97 promotes GSC self-renewal and tumorigenicity via mTORC2/AKT signaling. Thus, our findings suggest that CD97 may be a general GSC enrichment marker in GBM and that the CD97-related pathway might serve as a therapeutic target for GBM.

2024-12-03 | GSE201960 | GEO

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

Structural basis for CD97 recognition of the decay-accelerating factor CD55 suggests mechanosensitive activation of adhesion GPCRs.

Project description:The adhesion G protein-coupled receptor CD97 and its ligand complement decay-accelerating factor CD55 are important binding partners in the human immune system. Dysfunction in this binding has been linked to immune disorders such as multiple sclerosis and rheumatoid arthritis, as well as various cancers. Previous literatures have indicated that the CD97 includes 3 to 5 epidermal growth factor (EGF) domains at its N terminus and these EGF domains can bind to the N-terminal short consensus repeat (SCR) domains of CD55. However, the details of this interaction remain elusive, especially why the CD55 binds with the highest affinity to the shortest isoform of CD97 (EGF1,2,5). Herein, we designed a chimeric expression construct with the EGF1,2,5 domains of CD97 and the SCR1-4 domains of CD55 connected by a flexible linker and determined the complex structure by crystallography. Our data reveal that the two proteins adopt an overall antiparallel binding mode involving the SCR1-3 domains of CD55 and all three EGF domains of CD97. Mutagenesis data confirmed the importance of EGF5 in the interaction and explained the binding specificity between CD55 and CD97. The architecture of CD55-CD97 binding mode together with kinetics suggests a force-resisting shearing stretch geometry when forces applied to the C termini of both proteins in the circulating environment. The potential of the CD55-CD97 complex to withstand tensile force may provide a basis for the mechanosensing mechanism for activation of adhesion G protein-coupled receptors.

| S-EPMC8191316 | biostudies-literature

Effect of CD97 knockdown or overexpression in patient-derived GBM cultures (PDGCs)

Project description:To investigate differentially expressed genes upon CD97 manipulation in GBM

2023-12-01 | GSE230393 | GEO

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

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