Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Microarray analysis of colon tissue of DSS colitis STAP-2 KO mice

ABSTRACT: To identify STAP-2 regulating genes modulated intestine inflammation, we conducted microarray analyses using colon tissue from pooled WT (n=3) or STAP-2-/- mice (n=3) treated with DSS for 3 days. Bioinformatic analyses revealed that STAP-2 deletion mediates insufficient immune and inflammatory reaction through altering a series of associated gene expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE48543 | GEO | 2014/04/17

SECONDARY ACCESSION(S): PRJNA210513

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Microarray analysis of colon tissue of DSS colitis STAP-2 KO mice

Project description:To identify STAP-2 regulating genes modulated intestine inflammation, we conducted microarray analyses using colon tissue from pooled WT (n=3) or STAP-2-/- mice (n=3) treated with DSS for 3 days. Bioinformatic analyses revealed that STAP-2 deletion mediates insufficient immune and inflammatory reaction through altering a series of associated gene expression. The DSS-treated colons derived from WT (n=3) and STAP-2 KO (n=3) mice were examined. Each strain was run in biological duplicate.

2014-04-17 | E-GEOD-48543 | biostudies-arrayexpress

STAP-1 is Required for Maintenance of Leukemic Stem Cells in Chronic Myeloid Leukemia.

Project description:The family of signal transduction adapter proteins (STAPs) has been reported to be involved in a variety of intracellular signaling and transcriptional molecules. We originally cloned STAP-2 as a c-fms interacting protein and found the effects on chronic myeloid leukemia (CML) leukemogenesis. STAP-2 binds to BCR-ABL, up-regulates BCR-ABL phosphorylation and activates its downstream molecules. In this study, we evaluated the role of STAP-1, another member of the family, in CML pathogenesis. The expression of human STAP-1 is aberrantly upregulated in CML stem cells (LSCs) in patient bone marrow. Using experimental model mice, we revealed that deletion of STAP-1 prolonged survival of CML mice with the induced apoptosis of LSCs. The impaired phosphorylated status of STAT5 by STAP-1 ablation results in downregulation of anti-apoptotic genes, BCL-2 and BCL-xL. Interestingly, transcriptome analyses indicate that STAP-1 affects several signaling pathways related to BCR-ABL, JAK2 as well as PPARγ. This adaptor protein directly binds not only BCR-ABL, also STAT5 proteins, showing synergistic effects of STAP-1 inhibition on the treatment with BCR-ABL or JAK2 tyrosine kinase inhibitor. It is known that the inhibition of BCR-ABL alone cannot eliminate CML LSCs. Our results have identified STAP-1 as a regulator of CML LSCs and support the evidence as a novel therapeutic target for CML cure.

2020-07-15 | GSE127984 | GEO

DSS induced colitis mice Astral-DIA

Project description:This study aims to investigate the protein expression profiles in a murine model of dextran sulfate sodium (DSS)-induced colitis using advanced Astral-DIA quantitative proteomics technology. A total of 12 colon tissue samples were analyzed, including 6 from healthy control mice and 6 from DSS-treated mice with induced colitis. Experimental Design Species: Mus musculus (C57BL/6 strain). Tissue Source: Colon tissues were dissected, snap-frozen in liquid nitrogen, and homogenized to extract proteins. Groups: Control Group: Healthy mice without intervention. DSS Group: Mice subjected to 2.5% DSS administration for 7 days to induce colitis, validated by histopathological assessment.

2025-09-18 | PXD063633 | Pride

Colon gene expression signatures in wild type and Card9-/-mice exposed to DSS induced colitis

Project description:It is crucial to decipher the host-microbiota interactions as they are involved in intestinal homeostasis and diseases. Caspase Recruitment Domain 9 (Card9) is an inflammatory bowel disease (IBD) susceptibility gene coding for an adapter protein for innate immunity toward many microorganisms. Card9 mediates colitis recovery via interleukin 22 pathway activation and Card9-/- mice have enhanced susceptibility to colitis. To reveal the mechanisms responsible of this defect in Card9-/-mice, we compared colon transcriptomics in WT and Card9-/- mice before and during DSS-induced colitis. Mice transcriptomes clusterized according to the genotype supporting a pattern clearly different in WT and Card9-/- mice. The number of up-regulated genes at day 7 was largely higher in Card9-/- compared to WT mice. Pathway analyses of the induced transcripts showed a dominance of immune-related pathway with a stronger signal in Card9-/- mice. Interestingly, NOD-like receptor signaling pathway, in which CARD9 is involved, was an exception with weaker activation in Card9-/- than in WT mice. During the recovery period at day 12, pathways involved in cell proliferation and replication were significantly activated in WT compared to Card9-/- mice confirming the healing defect in Card9-/- mice. For the induction of colitis, mice were given drinking water supplemented with 2% (w/v) Dextran sulphate sodium (DSS) for 7 days, then allowed to recover by drinking water alone for 5 additional days. 3 mice of each groups (WT and Card9-/-) were sacrified before DSS administration. 5 WT mice and 4 Card9-/- mice were sacrified 7 days after DSS administration and 5 mice of each group were sacrified at day 12.

2016-04-05 | E-GEOD-67577 | biostudies-arrayexpress

Cell atlas of colon tissue from DSS-induced colitis mouse

Project description:Inflammation markedly alters the microenvironment of intestinal tissue. To explore alterations in the cell composition and transcription of intestinal tissue during colitis, we conducted single-cell RNA sequencing analysis of the colonic tissues obtained from the mice treated with 3% DSS for 6 days.

2024-05-28 | GSE268235 | GEO

Transcriptional profiling of murine distal colon from C57BL/6 (WT) and Stat2KO mice during acute DSS colitis.

Project description:Experimental colitis was induced in mice by the administration of 2% (w/v) Dextran sulfate sodium salt (DSS, colitis grade, 36-50kDa, MP Biomedicals) in the drinking water for 7 days followed by normal drinking water w/o DSS. Distal colons were collected two days later.

2023-10-01 | E-MTAB-12655 | biostudies-arrayexpress

Colon tissue lysates from DSS-induced acute colitis in Twist2Cre;Lkb1fl/+ or Lkb1fl/+ mice

Project description:Mice were exposed to 3% DSS in the drinking water for 7 days followed by 3 days of recovery. Colon tissues were collected at 3 day after recovery in RNA later and RNA was extracted using DNA, RNA, protein purification kit from Macherey-Nagel.

2024-07-24 | E-MTAB-13631 | biostudies-arrayexpress

Expression data from colon epithelium of STAT3IEC-KO in acute DSS colitis

Project description:STAT3 is a pleiotropic transcription factor with important functions in cytokine signalling in a variety of tissues. However, the role of STAT3 in the intestinal epithelium is not well understood. Here we demonstrate that development of colonic inflammation is associated with the induction of STAT3 activity in intestinal epithelial cells (IEC). Studies in genetically engineered mice showed that epithelial STAT3 activation in DSS colitis is dependent on IL-22 rather than IL-6. IL-22 was secreted by colonic CD11c+ cells in response to Toll-like receptor stimulation. Conditional knockout mice with an IEC specific deletion of STAT3 activity were highly susceptible to experimental colitis, indicating that epithelial STAT3 regulates gut homeostasis. STAT3IEC-KO mice, upon induction of colitis, showed a striking defect of epithelial restitution. Gene chip analysis indicated that STAT3 regulates the cellular stress response, apoptosis and pathways associated with wound healing in IEC. Consistently, both IL-22 and epithelial STAT3 were found to be important in wound-healing experiments in vivo. In summary, our data suggest that intestinal epithelial STAT3 activation regulates immune homeostasis in the gut by promoting IL-22-dependent mucosal wound healing. 4 samples of colon epithelium were analyzed from 4 mice (2 per group Stat3flfl VillinCre- and Stat3flfl VillinCre+, respectively) after they had been treated with DSS (2.5%) for 5 days

2009-05-08 | E-GEOD-15955 | biostudies-arrayexpress

TFEB target in epithelial cells during DSS colitis

Project description:TFEB in IEC has a protective role in DSS colitis. The goal is to examine what genes/pathways are TFEB target during DSS colitis

2018-02-22 | GSE98266 | GEO

Transcriptional profiling of murine distal colon from C57BL/6 (WT), Il20KO, Il20raKO and Il20rbKO mice during acute DSS colitis

Project description:Experimental colitis was induced in mice by the administration of 1.5% (w/v) Dextran sulfate sodium salt (DSS, colitis grade, 36-50kDa, MP Biomedicals) in the drinking water for 7 days followed by normal drinking water w/o DSS. Distal colons were collected two days later.

2023-10-01 | E-MTAB-12737 | 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