Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human-Specific Elimination of Epithelial Siglec-XII Suppresses the Risk of CRC Initiation and Progression [baseline]

ABSTRACT: Human-Specific Elimination of Epithelial Siglec-XII Suppresses the Risk of CRC Initiation and Progression [baseline]

PROVIDER: PRJNA1090163 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28401416_1.fastq.gz	Fastqsanger.gz
	SRR28401416_2.fastq.gz	Fastqsanger.gz
	SRR28401417_1.fastq.gz	Fastqsanger.gz
	SRR28401417_2.fastq.gz	Fastqsanger.gz
	SRR28401418_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Human-Specific Elimination of Epithelial Siglec-XII Suppresses the Risk of CRC Initiation and Progression [baseline]

Project description:Human-specific changes in specific Siglecs is one of the reasons put forth as molecular mechanisms that could explain human proneness to developing cancers. The SIGLEC12 gene, which encodes the Siglec-XII protein mainly found on epithelial cells, has a fixed homozygous missense mutation in a critical arginine renders unable to recognize its natural ligand. Additionally, the gene harbors a polymorphic frameshift mutation that eliminates expression of the full-length protein in most humans. We hypothesized that dysfunctional Siglec-XII is involved in cancer progression in humans' epithelia. Here we report that the transgenic conditional expression of human Siglec-XII in mouse intestinal epithelia did not by itself cause carcinomas and RNA sequencing of the colons at baseline derived a gene signature without differentially expressed genes (DEGs) between controls (Villin1-Cre-ER(T2)) and Siglec-XII-expressing mice

2024-03-27 | GSE262086 | GEO

Human-Specific Elimination of Epithelial Siglec-XII Suppresses the Risk of CRC Initiation and Progression [ENDPOINT]

Project description:Human-specific changes in specific Siglecs is one of the reasons put forth as molecular mechanisms that could explain human proneness to developing cancers. The SIGLEC12 gene, which encodes the Siglec-XII protein mainly found on epithelial cells, has a fixed homozygous missense mutation in a critical arginine renders unable to recognize its natural ligand. Additionally, the gene harbors a polymorphic frameshift mutation that eliminates expression of the full-length protein in most humans. We hypothesized that dysfunctional Siglec-XII is involved in cancer progression in humans' epithelia. Here we report that the transgenic conditional expression of human Siglec-XII in mouse intestinal epithelia increased the number and size of cancers in a model of colitis-associated colorectal carcinoma (AOM/DSS). RNA sequencing of the colons at baseline and after AOM/DSS challenge derived a gene signature comprised of the differentially expressed genes (DEGs) between controls (Villin1-Cre-ER(T2)) and Siglec-XII-expressing mice, showing that upregulated DEGs in Siglec-XII mice were enriched for diverse bioenergetic processes.

2024-03-27 | GSE262087 | GEO

Human-Specific Elimination of Epithelial Siglec-XII Suppresses the Risk of CRC Initiation and Progression [CACO]

Project description:Human-specific changes in specific Siglecs is one of the reasons put forth as molecular mechanisms that could explain human proneness to developing cancers. The SIGLEC12 gene, which encodes the Siglec-XII protein mainly found on epithelial cells, has a fixed homozygous missense mutation in a critical arginine renders unable to recognize its natural ligand. Additionally, the gene harbors a polymorphic frameshift mutation that eliminates expression of the full-length protein in most humans. We hypothesized that dysfunctional Siglec-XII is involved in cancer progression in humans' epithelia. Here we report that the forced expression of human Siglec-XII in caco-2 cells showed that differentially expressed genes in Siglec-XII cells were enriched for diverse bioenergetic processes.

2024-03-27 | GSE262085 | GEO

Human-Specific Elimination of Epithelial Siglec-XII Suppresses the Risk of CRC Initiation and Progression

Project description:Human-Specific Elimination of Epithelial Siglec-XII Suppresses the Risk of CRC Initiation and Progression

| PRJNA1090166 | ENA

Human-Specific Elimination of Epithelial Siglec-XII Suppresses the Risk of CRC Initiation and Progression [ENDPOINT]

Project description:Human-Specific Elimination of Epithelial Siglec-XII Suppresses the Risk of CRC Initiation and Progression [ENDPOINT]

| PRJNA1090216 | ENA

Human-Specific Elimination of Epithelial Siglec-XII Suppresses the Risk of CRC Initiation and Progression [CACO]

Project description:Human-Specific Elimination of Epithelial Siglec-XII Suppresses the Risk of CRC Initiation and Progression [CACO]

| PRJNA1090164 | ENA

Human CRC cell line baseline phosphoproteomics

Project description:There is a need for robust phosphopeptide enrichment methods to allow signaling network analysis in cancer cell lines and tissues with minimal fractionation. With recent instrument developments thousands of unique phosphopeptides can be detected by single-shot LC-MS/MS. However, successful phosphoproteomics experiments still rely on efficient phosphopeptide enrichment from a tryptic digest prior to LC-MS/MS analysis. Here we describe a performance assessment of HAMMOC (hydroxyl acid modified metal affinity chromatography) (Sugiyama MCP2007, Kyono, JPR 2008) combined with single shot label-free quantitation at 500 µg peptide input level. We apply the method to profile the baseline phosphorylation landscape of a panel of 8 colorectal cancer (CRC) cell lines. These CRC cell lines represent the 3 CRC subtypes (CCS1, CCS2 and CCS3) as reported by large-scale transcriptome analysis. We report an analysis of the phosphoprotein network and processes enriched in the cell lines representing the poor prognosis CCS3 subtype.

2015-04-15 | PXD001550 | Pride

Human-Specific Elimination of Epithelial Siglec-XII Suppresses the Risk of CRC Initiation and Progression

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

2024-03-27 | GSE262088 | GEO

Human CRC cell line baseline phosphoproteomics

2017-03-29 | MSV000080788 | MassIVE

Ablation of collagen XII disturbs joint extracellular matrix organization and causes patellar subluxation

Project description:Collagen XII, belonging to the fibril-associated collagens, is a homotrimeric secreted extracellular matrix (ECM) protein encoded by the COL12A1 gene. Mutations in the human COL12A1 gene cause an Ehlers-Danlos/myopathy overlap syndrome leading to skeletal abnormalities and muscle weakness. Here, we studied the role of collagen XII in joint pathophysiology by analyzing collagen XII deficient mice and human patients. We found that collagen XII is widely expressed across multiple connective tissue of the developing joint. Lack of collagen XII in mice destabilizes tendons and the femoral trochlear groove to induce patellar subluxation in the patellofemoral joint. These changes are associated with an ECM damage response in tendon and secondary quadriceps muscle degeneration. Moreover, patellar subluxation was also identified as a clinical feature of human patients with collagen XII deficiency. The results provide an explanation for joint hyperlaxity in mice and human patients with collagen XII deficiency.

2023-06-19 | GSE234964 | 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