Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiles of Treg cells lacking Cdc42 GTPase

ABSTRACT: Treg cells play an important role in immune tolerance and tumor immune evasion through suppression of effector T cells. Treg cell lineage instability may be harnessed to trigger anti-tumor T cell immunity. However, the mechanism underlying Treg cell stability remains poorly understand. By characterizing Treg cell-specific heterozygous and homozygous Cdc42 knockout mice, we found that Cdc42 is essential for Treg cell stability. By RNA sequencing of heterozygous and homozygous Cdc42 knockout Treg cells, we found that Cdc42 maintains Treg cell stability through suppression of carbonic anhydrase I (CAI) expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE181779 | GEO | 2021/08/12

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression profiles of Treg cells lacking Cdc42 GTPase

Project description:Gene expression profiles of Treg cells lacking Cdc42 GTPase

| PRJNA753464 | ENA

Roles of Cdc42 and Rac in Bergmann glia during cerebellar corticogenesis (WT_primary_astrocyte)

Project description:Bergmann glia (BG) are important in the inward type of radial migration of cerebellar granule neurons (CGNs). However, details regarding the functions of Cdc42 and Rac in BG for radial migration of CGN are unknown. To examine the roles of Cdc42 and Rac in BG during cerebellar corticogenesis, mice with a single deletion of Cdc42 or Rac1 and those with double deletions of Cdc42 and Rac1 under control of the glial fibrillary acidic protein (GFAP) promoter: GFAP-Cre;Cdc42flox/flox (Cdc42-KO), GFAP–Cre;Rac1flox/flox (Rac1-KO), and GFAP-Cre;Cdc42 flox/flox;Rac1flox/flox (Cdc42/Rac1-DKO) mice, were generated. Both Cdc42-KO and Rac1-KO mice, but more obviously Cdc42-KO mice, had disturbed alignment of BG in the Purkinje cell layer (PCL). We found that Cdc42-KO, but not Rac1-KO, induced impaired radial migration of CGNs in the late phase of radial migration, leading to retention of CGNs in the inferior half of the molecular layer (ML). Cdc42-KO, but not Rac1-KO, mice also showed aberrantly aligned Purkinje cells (PCs). These phenotypes were exacerbated in Cdc42/Rac1-DKO mice. Alignment of BG radial fibers in the ML and BG endfeet at the pial surface of the cerebellum evaluated by GFAP staining was disturbed and weak in Cdc42/Rac1-DKO mice, respectively. Our data indicate that that Cdc42 and Rac, but predominantly Cdc42, in BG play important roles during the late phase of radial migration of CGNs. We also report here that Cdc42 is involved in gliophilic migration of CGNs, in contrast to Rac, which is more closely connected to regulating neurophilic migration.

2018-01-01 | GSE106141 | GEO

Cdc42 controls DC-maturation - Cdc42-dependent actin dynamics controls maturation and secretory activity of dendritic cells

Project description:Cell division cycle 42 (Cdc42) is a member of the Rho GTPase family and has pivotal functions in actin organization, cell migration and proliferation. Cdc42 has been shown to regulate antigen (Ag)-uptake in immature dendritic cells (DC) and controls their migration from tissues to lymph nodes. Previous reports demonstrated that Cdc42 is inactivated upon DC-maturation to avoid continued Ag-acquisition. To further study the molecular mechanisms of DC-control by Cdc42, we used bone marrow-derived DCs from Cdc42-deficient mice. We show that Cdc42-deficient DCs are phenotypically mature without additional maturation stimuli, as they upregulate CD86 from intracellular storages to the cell surface. They also accumulate invariant chain (Ii)-MHC class II complexes at the cell surface, which cannot efficiently present peptide Ag for priming of Ag-specific CD4 T cells. Lack of Cdc42 in immature DCs does not allow MHC class II maturation, as lysosomal Cathepsins are lost into the supernatant and Ii-MHC class II complexes cannot mature. Therefore Cdc42-deficient DCs are "pseudomature" and lose most functional hallmarks of antigen-presenting cells. Our results propose that Cdc42 keeps DCs in an immature state, while downregulation of Cdc42-activity during maturation facilitates generation of CD86+MHCII+ mature DCs.

2015-10-12 | PXD001934 | Pride

Gene expression changes in REH following CDC42 inhibition

Project description:ARHGEF4 expression is associated with t(12;21) acute lymphoblastic leukaemia (ALL). Our study investigated the substrate specificity of ARHGEF4, a member of the diffuse B-cell lymphoma (DBL) family of guanine nucleotide exchange factors (GEFs), in t(12;21) ALL REH cells. ARHGEF4 was found to activate the small guanine nucleotide binding protein (GTPase) CDC42. In order to determine the function of CDC42 in t(12;21) ALL cells, we performed RNAseq analysis on REH cells treated for 24 hours with DMSO vehicle control in comparison to 25uM ML141, a CDC42 inhibitor.

2020-06-20 | GSE152836 | GEO

Roles of Cdc42 and Rac in Bergmann glia during cerebellar corticogenesis (U87_CDC42RAC1-DKD)

2018-01-01 | GSE106142 | GEO

Transport of influenza A virus neuraminidase to host cell surface and virus replication are regulated by ARHGAP21 and Cdc42

Project description:Influenza virus neuraminidase (NA), a type II transmembrane glycoprotein, is transported to the virus assembly site at the plasma membrane and is a major viral envelope component that plays a critical role in the release of progeny virions and in determination of host range restriction. Although signals/sequences in NA for translocation, sorting and raft association have been identified, little is known about the host factors that are involved in regulating the intracellular and cell surface transport of NA. In this report, we have investigated the involvement of Rho family GTPases in NA transport to the cell surface. We found that expression of constitutively active or inactive mutants of RhoA or Rac1 did not significantly affect the amount of NA that reached the cell surface. Interestingly, expression of constitutively active Cdc42 or depletion of the Cdc42-specific GAP, ARHGAP21, promoted the transport of NA to the plasma membranes. By contrast, cells expressing shRNA targrting Cdc42 or overexpressing ARHGAP21 exhibited a significant decrease in the amount of cell surface-localized NA. Furthermore, silencing of Cdc42 or ARHGAP21 had significant effects on influenza A virus replication. Together, our results reveal that ARHGAP21 and Cdc42-based signaling regulates the NA transport and thereby impacts virus replication. This microarray experiment was carried out to find out whether Cdc42 and ARHGAP21 expression levels in A549 cell were changed after WSN infection. Total RNAs were extracted from three different groups of A549 cells that had been infected with or without WSN for 10 h, using TRIzol reagent (Invitrogen, Carlsbad, CA). Samples were amplified and labeled using a NimbleGen One-Color DNA Labeling Kit.

2012-04-03 | E-GEOD-32878 | biostudies-arrayexpress

Cdc42 phosphorylation study - Cdc42 Regulates Neuronal Polarity during Cerebellar Axon Formation and Glial-Guided Migration

Project description:Govek et al. demonstrate conditional loss of Cdc42 in cerebellar granule cell progenitors (GCPs) perturbs GCP polarity and impairs axon patterning, glial-guided migration, and cerebellar foliation. Phospho-proteomic analysis identified polarity and cytoskeletal proteins as affected targets in Cdc42 deficient GCPs.

2018-10-22 | PXD008148 | Pride

CTLA4 haploinsufficiency and immune dysregulation

Project description:We identified germline heterozygous mutations in CTLA4 in members of four families with severe immune dysregulation. Human CTLA4 haploinsufficiency caused dysregulation of FoxP3+ regulatory T (Treg) cells and lymphocytic infiltration of target organs, mimicking Ctla4 homozygous mice. Patients also exhibited a B cell phenotype, with progressive loss of B cells and accumulation of autoreactive CD21lo B cells. This study demonstrates a critical quantitative role for CTLA-4 in human immune homeostasis.

| phs000797 | dbGaP

CDC42 controlled apical-basal polarity regulates intestinal stem cell to transit amplifying cell fate transition via YAP-EGF-mTOR signaling

Project description:Epithelial polarity is controlled by a polarity machinery including the Rho GTPase CDC42 and Scribble/PAR. By using intestinal stem cell (ISC)-specific deletion of CDC42 in Olfm4-IRES-eGFPCreERT2;CDC42flox/flox mice, we found that ISC-initiated CDC42 loss caused a drastic hyper-proliferation of transit amplifying (TA) cells and disrupted epithelial polarity. CDC42-null crypts displayed expanded TA cell and diminished ISC populations, accompanied by elevated hippo signaling via YAP/TAZ - Ereg and mTOR activation, independent from canonical Wnt signaling. YAP/TAZ conditional knockout restored the balance of ISC/TA cell populations and crypt proliferation but did not rescue the polarity in CDC42-null small intestine. mTOR or EGFR inhibitor treatment of CDC42 KO mice exhibited similar rescuing effects without affecting YAP/TAZ signaling. Inducible ablation of Scribble in intestinal epithelial cells mimics that of CDC42 KO defects including crypt hyperplasia and hippo signaling activation. Mammalian epithelial polarity regulates ISC and TA cell fate and proliferation via a hippo-Ereg-mTOR cascade.

2021-10-23 | GSE166736 | GEO

Expression data from sorted Treg cells from WT or motheaten mice

Project description:The importance of regulatory T cells (Treg) for immune tolerance is well recognized, yet the signaling molecules influencing their suppressive activity are relatively poorly understood. We identified the cytoplasmic tyrosine phosphatase SHP-1 as a novel ‘endogenous brake’ and modifier of the suppressive ability of Treg cells; consistent with this notion, loss of SHP-1 expression strongly augments the ability of Treg cells to suppress inflammation in a mouse model. Specific harmacological inhibition of SHP-1 enzymatic activity via the cancer drug sodium stibogluconate (SSG) potently augmented Treg cell suppressor activity both in vivo and ex vivo. We evaluated the gene expression profiles of sorted T reg cells (CD4+CD25+) from wild type (wt) mice and mice that were heterozygous (he) or homozygous (me) for SHP-1 knockout (motheaten phenotype). T reg (CD4+CD25+) cells were isolated form wild type (WT) mice and that were heterozygous (he) or homozygous (me) for SHP-1 knockout (motheaten phenotype); totalRNA was isolated using Arcturus reagents; aRNA was generated and amplified using Arcturus reagents; and labeled product was hybridized to Affymetrix chips to asses gene expression patterns.

2010-08-13 | E-GEOD-23600 | biostudies-arrayexpress

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