Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq profiling of ADAM10 inhibition in DLD-1 and SW620 colorectal cancer cell lines

ABSTRACT: This study examines the transcriptomic effects of ADAM10 inhibition in two human colorectal cancer cell lines, DLD-1 and SW620. Cells were treated with vehicle control or the conformation-specific ADAM10 monoclonal antibody 1H5 for 48 hours, followed by extraction of total RNA and paired-end RNA sequencing. The dataset enables comparative analysis of ADAM10-regulated pathways across different CRC genetic backgrounds, including alterations in Notch and EGFR signaling, metabolic gene programs, and other pathways associated with tumor progression.

ORGANISM(S): Homo sapiens

PROVIDER: GSE311253 | GEO | 2026/01/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-seq profiling of ADAM10 inhibition in DLD-1 and SW620 colorectal cancer cell lines

Project description:RNA-seq profiling of ADAM10 inhibition in DLD-1 and SW620 colorectal cancer cell lines

| PRJNA1368855 | ENA

Expression data from Adam10 knock out mice and wild type

Project description:Adam10, a cell surface protease, cleaving many proteins including TNF-alpha and E-cadherin. Here we investigate the genome wide effects of Adam10 knock out on the transcriptome. Commercial microarrays (Affymetrix Mouse Gene ST 1.0) were used to generate genome wide mRNA profiles. Mouse tissue samples from n=4 wiltype skin and n=4 Adam10 knockout skin were used in the study.

2011-01-06 | E-GEOD-25480 | biostudies-arrayexpress

Tetraspanin Tspan15 is an essential subunit of an ADAM10 scissor complex

Project description:A disintegrin and metalloprotease 10 (ADAM10) is essential for embryonic development and impacts on diseases such as cancer, Alzheimer’s and inflammatory diseases. ADAM10 is a ‘molecular scissor’ that proteolytically cleaves the extracellular region from over 100 substrates, including Notch, amyloid precursor protein, cadherins, growth factors and chemokines. ADAM10 was recently proposed to function as six distinct scissors with different substrates, depending on its association with one of six regulatory tetraspanins, termed TspanC8s. However, it remains unclear whether ADAM10 function is critically dependent on a TspanC8 partner. To address this, we generated the first monoclonal antibodies to Tspan15 as a model TspanC8. These were used to show that ADAM10 is the principal Tspan15-interacting protein, that Tspan15 expression requires ADAM10 in cell lines and primary cells, and that a synthetic ADAM10/Tspan15 fusion protein is a functional scissor. Together these findings suggest that ADAM10 exists as an ADAM10/TspanC8 scissor complex.

2021-08-24 | PXD016508 | Pride

Single cell analysis of SW620/SW620-TET2CD with long time clone culturing

Project description:In order to understand the single cell nature of SW620/SW620-TET2CD, we used the SW620/SW620-TET2CD clone from Day6/Day9/Day12/Day15 to start our single cell sequencing and analysis the diffference of single cell gene expression from different samples.

2024-11-01 | GSE188329 | GEO

Murine cartilage tissues (tibia): Control vs ADAM10 flox/flox-Col2a1-Cre

Project description:Transcriptional profiling of mouse cartilage tissues comparing control and mutant mice (in which the Adam10 allele was excised under the control of a Col2a1 promoter) to negate ADAM10 activity in osteochondroprogenitors. Goal was to determine the effects of the loss of ADAM10 activity on cartilage gene expression.

2019-12-11 | GSE141743 | GEO

Expression data from SW620/sh control and SW620/shMACC1

Project description:Expression data from SW620/sh control and SW620/shMACC1

| PRJNA734527 | ENA

Differential gene expression in ADAM10 over-expressing transgenic mice

Project description:In a transgenic mouse model of Alzheimer disease (AD), cleavage of the amyloid precursor protein (APP) by the α-secretase ADAM10 prevented amyloid plaque formation and alleviated cognitive deficits. Furthermore, there was a positive influence of ADAM10 over-expression on neurotransmitter-specific formation of synapses and on synaptic plasticity. To assess the influence of ADAM10 on the gene expression profile in the brain we performed microarray analysis using RNA isolated from brains of five month old mice over-expressing either the α-secretase ADAM10 or a dominant-negative mutant (dn) of this enzyme. As compared to non-transgenic wild-type mice, 355 genes were found to be differentially expressed in ADAM10 transgenic mice and 143 genes in dnADAM10 mice. A higher number of genes was found to be differentially regulated in double-transgenic mouse strains additionally expressing the human APP V717I mutant (APP[V717I]). Thus, α-secretase cleavage of over-expressed APP[V717I] alters CNS gene expression additionally. Keywords: genetic modification

2009-01-22 | GSE10908 | GEO

Expression data from Adam10 knock out mice and wild type

2011-01-06 | GSE25480 | GEO

HMGA2-driven gene expression in human colorectal DLD-1 cells.

Project description:Gene expression analysis of stable HMGA2-overexpressing DLD-1 cells (DLD-1-HMGA2) and its control cells (DLD-1-Vector).

2019-08-29 | GSE136544 | GEO

Targeting cardiomyocyte ADAM10 ectodomain shedding promotes survival early after myocardial infarction

Project description:Myocardial infarction (MI) contributes to cardiac mortality and morbidity. After myocardial infarction the innate immune response is pivotal in clearing of tissue debris as well as scar formation, but exaggerated cytokine and chemokine secretion with subsequent leukocyte infiltration also leads to further tissue damage. Post-translational regulation of cytokine / chemokine signaling occurs via ectodomain shedding through a disintegrin and metalloproteases (ADAMs). Here, we address the value of targeting a previously unknown ADAM10 / CX3CL1 axis in the regulation of neutrophil recruitment early after MI. We show that myocardial ADAM10 is distinctly upregulated in biopsies from patients with ischemia-driven cardiomyopathy and correlates with heart failure progression. Intriguingly, upon MI in mice, pharmacological treatment with the ADAM10 inhibitionor GI254023X as well as genetic cardiomycyte-specific ADAM10 deletion improves survival with markedly enhanced heart function and reduced scar size. Mechanistically, this is driven by abolished ADAM10-mediated CX3CL1 ectodomain shedding followed by diminished IL-1β-dependent inflammation, reduced neutrophil bone marrow egress as well as myocardial tissue infiltration. Genetic cardiomycyte-specific ADAM10 deletion confirmes the small-molecule data and leads to improved cardiac function and reduction in inflammatory markers after ischemic myocardial injury. Thus, our data shows a conceptual insight into how acute MI induces chemotactic signaling via ectodomain shedding in cardiomyocytes.

2022-11-10 | GSE217268 | 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