Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The gene expression effects of DSG2 knockout in A431 epidermoid cell line

ABSTRACT: The gene expression effects of DSG2 knockout in A431 epidermoid cell line

PROVIDER: PRJNA1298353 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

The gene expression effects of DSG2 knockout in A431 epidermoid cell line

Project description:Desmogleins are transmembrane cadherin proteins and obligate members of the desmosome, a cell-cell adhesion complex which connects adjacent cells and provides structural integrity to tissues. While Desmogleins are well-known for their importance in maintenance of cell-cell junctions, several studies have also highlighted their role in signaling crosstalk with cell-matrix adhesions and the extracellular matrix (ECM). We have recently shown that Desmoglein-2 (Dsg2) controls cell spreading on ECM substrates (fibronectin and collagen) and phosphorylation of focal adhesion proteins via Rap1 GTPase signaling. In our current study, we show that loss of Dsg2 in keratinocytes enhances the expression of ECM proteins and matrix metalloproteinases (MMPs), an effect that was not recapitulated upon loss of Desmocollin-2 (Dsc2) or loss of Dsg2 in other epithelial cell types. Signaling pathways well-known to control ECM function (TGF-B and Rho) were shown to have no effect on Dsg2-mediated changes in ECM and MMP gene expression, but an analysis of global transcriptome changes by RNA sequencing identified major changes in NF-kappaB (NF-KB)-mediated signaling in Dsg2-deficient cells. Interestingly, NF-KB (RelA) activation is elevated in Dsg2-deficient cells, and knockdown of RelA rescued both the enhanced expression of ECM/MMP genes and the enhanced migratory ability of Dsg2-deficient cells. Taken together, this study has identified an important link between Dsg2 and NF-KB signaling involved in controlling matrix production and remodeling, which has relevance for multiple processes in the epidermis such as wound healing and psoriasis.

2025-08-20 | GSE303980 | GEO

human epidermoid carcinoma cell: Control (A431-P cells) vs. highly invasive subline (A431-III cells)

Project description:Transcriptional profiling of human epidermoid carcinoma cell comparing control A431-P cells with highly invasive subline A431-III cells

2013-06-18 | GSE47996 | GEO

human epidermoid carcinoma cell: Control (A431-P cells) vs. highly invasive subline (A431-III cells)

Project description:Transcriptional profiling of human epidermoid carcinoma cell comparing control A431-P cells with highly invasive subline A431-III cells No treatmentt, A431-P cells vs. A431-III cells. A431-P cells are used as a reference to invstigate A431-III cells.

2013-06-18 | E-GEOD-47996 | biostudies-arrayexpress

Transcriptome profiling of RBM3 overexpression in A431 cells

Project description:This study aims to investigate the transcriptional changes induced by overexpression of RNA-binding protein RBM3 in A431 human epidermoid carcinoma cells. Lentiviral transduction was used to stably overexpress RBM3 in A431 cells. Total RNA was extracted from RBM3 overexpressing cells and control cells, followed by RNA-seq library preparation and sequencing on Illumina platform. Differential gene expression analysis will be performed to identify RBM3 targets and regulatory networks.

2025-05-01 | GSE264600 | GEO

RNA-Sequencing of heart tissue obtained from cardiac specific-Dsg2-/- and wild-type (Dsg2+/+) mice at 2-weeks and 10-weeks of age

Project description:We studied how loss of the desmosome associated protein, desmoglein-2 (Dsg2), in the heart leads to Arrhythmogenic Cardiomyopathy with particular interest in the early stages of disease progression. Mice expressing the cardiac αMHC-Cre promoter were crossed with Dsg2 floxed mice in which exon 4-5 of the Dsg2 gene was flanked by loxP sites, resulting in Cre-mediated excision of Dsg2 in cardiac myocytes. Wild type Dsg2+/+ (Cre-, Dsg2flx/flx) and knockout Dsg2-/- (Cre+, Dsg2flx/flx) mice were generated. RNA-seq was performed on heart tissue obtained from wild-type and Dsg2-/- mice at 2-weeks and 10-weeks of age.

2021-07-22 | GSE153124 | GEO

Transcriptomic analysis of DSG2-W2A mouse heart tissue

Project description:Transcriptomic analysis of DSG2-W2A mouse heart tissue. In DSG2-W2A mice, adhesion of the desmosomal molecule desmoglein-2 (DSG2) is abrogated via mutation of its’ major interaction mechanism (so-called "tryptophan swap" (Harrison, Brasch et al. 2016)). Adult DSG2-W2A mut/mut mice resemble the phenotype of Arrhythmogenic Cardiomyopathy (ACM or ARVC) with biventricular fibrosis, impaired systolic output function and arrhythmia. This phenotype was present in mutant mice analysed at the age of 9 weeks compared to 5-days old hearts, which showed no morphological alterations.

2022-12-05 | GSE181868 | GEO

RNA-seq of A431 cell line after gefitinib treatment

Project description:RNA-seq of A431 cell line after gefitinib treatment

| PRJEB18261 | ENA

Proximity Labeling and Genetic Screening Reveals the Role of DSG2/Siglec-9 Axis in Suppressing Macrophage Phagocytosis

Project description:In current study, we have established a combined strategy using proximity labeling and genetic screening to identify the cellular ligands of Siglec-9. Our use of proximity labeling using APEX2 fusion proteins followed by quantitative proteomics allowed us to efficiently label and enrich cell surface protein ligands that directly interact with Siglec-9 via sialic acid moieties. By combining with CRISPR knockout screening, we were able to identify functionally significant ligands. We confirmed at the cellular level that DSG2 expressed on cell surfaces directly interacts with Siglec-9, and this interaction is mediated by site-specific N-glycans on the ECD of DGS2. We also demonstrated the binding between DSG2 on A375 melanoma cells and Siglec-9 on macrophages contributes significantly to Siglec-9 signaling and blocking the DSG2-Siglec-9 axis by either DSG2 knockdown or anti-Siglec-9 antibody, releases immune-suppression and increases phagocytosis. Our findings revealed an important ligand in cancer cells for the immunosuppressive receptor Siglec-9, and suggest the potential of disrupting DSG2-Siglec-9 signaling axis in anti-cancer therapy.

2024-12-23 | PXD051557 | Pride

RNA-seq of A431 cell line after gefitinib treatment

Project description:RNA sequencing of A431 cell line samples before and after gefitinib treatment, at 0, 2, 6 and 24 hours, was performed in order to characterize the cell line's early and late response to this drug, and to compare against proteomics (mass spectrometry) characterization of the cell line using the same setup. These data were used in Branca et al., HiRIEF LC-MS enables deep proteome coverage and unbiased proteogenomics., Nat Methods. 2014 Jan;11(1):59-62 (doi: 10.1038/nmeth.2732).

2016-12-01 | E-MTAB-5285 | biostudies-arrayexpress

Expression data to parental A431 VS CD109 KO A431

Project description:Expression data to parental A431 VS CD109 KO A431

| PRJNA482298 | ENA