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Expression data of intestinal polyps and intestinal normal tissue from Ubc9+/+ and Ubc9+/- Villin-CreERT2 Apcf/+ mice 12 weeks after 4-OHT treatment

ABSTRACT: Expression data of intestinal polyps and intestinal normal tissue from Ubc9+/+ and Ubc9+/- Villin-CreERT2 Apcf/+ mice 12 weeks after 4-OHT treatment

PROVIDER: PRJNA609109 | ENA |

REPOSITORIES: ENA

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Expression data of intestinal polyps and intestinal normal tissue from Ubc9+/+ and Ubc9+/- Villin-CreERT2;Apcf/+ mice 12 weeks after 4-OHT treatment

Project description:Most human cancers present hyperactivated sumoylation, and cancer cell lines are usually highly sensitive to the lack of it, supporting potential application of sumoylation chemical inhibitors in cancer therapy. Here, we explored the impact of hyposumoylation (Ubc9 haploinsufficiency) on cancer development in mice using Apc loss-driven intestinal tumorigenesis model. We used microarrays to compare the global program of gene expression in intestinal polyps and normal tissue from mice homozygous (+/+) and heterozygous (+/-) for Ubc9, which encodes the unique SUMO E2-conjugating enzyme. This analysis was performed in the context of a conditional ablation of tumor suppressor Apc all along the crypt-villus axis through expresion of Cre recombinase driven by the intestinal specific promoter Villin

2020-09-14 | GSE146039 | GEO

Ubc9 overexpression and SUMO1 deficiency blunt inflammation after intestinal ischemia/reperfusion.

Project description:The intestinal epithelium constitutes a crucial defense to the potentially life-threatening effects of gut microbiota. However, due to a complex underlying vasculature, hypoperfusion and resultant tissue ischemia pose a particular risk to function and integrity of the epithelium. The small ubiquitin-like modifier (SUMO) conjugation pathway critically regulates adaptive responses to metabolic stress and is of particular significance in the gut, as inducible knockout of the SUMO-conjugating enzyme Ubc9 results in rapid intestinal epithelial disintegration. Here we analyzed the pattern of individual SUMO isoforms in intestinal epithelium and investigated their roles in intestinal ischemia/reperfusion (I/R) damage. Immunostaining revealed that epithelial SUMO2/3 expression was almost exclusively limited to crypt epithelial nuclei in unchallenged mice. However, intestinal I/R or overexpression of Ubc9 caused a remarkable enhancement of epithelial SUMO2/3 staining along the crypt-villus axis. Unexpectedly, a similar pattern was found in SUMO1 knockout mice. Ubc9 transgenic mice, but also SUMO1 knockout mice were protected from I/R injury as evidenced by better preserved barrier function and blunted inflammatory responses. PCR array analysis of microdissected villus-tip epithelia revealed a specific epithelial contribution to reduced inflammatory responses in Ubc9 transgenic mice, as key chemotactic signaling molecules such as IL17A were significantly downregulated. Together, our data indicate a critical role particularly of the SUMO2/3 isoforms in modulating responses to I/R and provide the first evidence that SUMO1 deletion activates a compensatory process that protects from ischemic damage.

2018-11-07 | GSE96733 | GEO

Expression data from FACS-purified Lgr5-EGFP+ intestinal cells from Ubc9+/+ and Ubc9+/- mice

Project description:The Lgr5+ intestinal stem cell, Paneth and transit-amplifying cell compartment constitute the intestinal crypt which is the constant source of differentiated epithelial cells that replenish the intestinal villi ensuring organ maintenance and regeneration. The Lgr5+ crypt-based columnar (CBC) cells have been identified as the intestinal stem cells (ISCs) and, importantly, as cells-of-origin of intestinal cancer. We used microarrays to detail the global program of gene expression in normal ISCs describing a mild downregulation of the sumoylation (post-translational modification (PTM) of proteins by SUMO) imposed by the loss of one allele of the unique E2-conjugating enzyme (Ubc9) of the pathway.

2020-09-14 | GSE146106 | GEO

Stool-derived 16s rRNA V4 sequencing from inducible intestinal-epithelium-LSD1-cKO mice (Villin-CreERT2+ Lsd1fl/fl (icKO)) against WT (Villin-CreERT2+ Lsd1fl/+ (icKO)) controls (before and 1-6 weeks after tamoxifen treatment)

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2023-10-31 | E-MTAB-12626 | biostudies-arrayexpress

Expression data from FACS-purified Lgr5-EGFP+ intestinal cells from Ubc9+/+ and Ubc9+/- mice

Project description:Expression data from FACS-purified Lgr5-EGFP+ intestinal cells from Ubc9+/+ and Ubc9+/- mice

| PRJNA609313 | ENA

Expression profiling of RFP-positive cells isolated from Ki67-RFP/Tcf7l2/Villin-CreERT2 mouse small intestinal epithelium 7 days after tamoxifen administration.

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2026-06-29 | E-MTAB-13606 | biostudies-arrayexpress

Gene expression data from crypts isolated from WT and Lpcat3 Villin-CreERT2 mice

Project description:We used microarray to analyze the global gene expression in crypts isolated from wild-type (Lpcat3F/F) and Lpcat3 tamoxifen inducible intestine-specific knockout (Lpcat3F/F, Villin-CreERT2) crypts. Phospholipid remodeling is a critical determinant of membrane composition and function. How membrane phospholipid composition affects tissue stem cell function and tumorigenesis is unknown. Here we demonstrate that Lpcat3-dependent phospholipid remodeling regulates intestinal stem cell (ISC) proliferation and promotes tumorigenesis in intestine. The objective of generating this dataset was to analyze the effects of Lpcat3 loss of function on gene expression in mouse intestine crypts.

2017-12-05 | GSE98516 | GEO

Single cell RNA-Seq expression profiling of RFP-positive cells isolated from Ki67-RFP/Tcf7l2/Villin-CreERT2 mouse small intestinal epithelium 7 days after tamoxifen administration

Project description:The T-cell factor 4 (Tcf4) protein (encoded by the Tcf7l2 gene) is a nuclear transcription regulator, which plays a key role in maintaining intestinal homeostasis, stem cell self-renewal and epithelial cell differentiation. Tcf4 has been identified as a key regulator of Paneth cell function in small intestinal crypts. It controls the expression of antimicrobial peptides and other effector molecules that contribute to the maintenance of the intestinal microbiota and protection against intestinal pathogens. Depletion of Tcf4 in mouse intestinal epithelial cells leads to loss of proliferating cells and dramatic changes in the morophology of the intestinal epithelum. To examine Tcf4 function in more detail, we used the Ki67-RFP Tcf7l2-flox/flox Villin-CreERT2 mouse strain. In this strain, proliferating cells are marked by expression of red fluorescent protein (RFP) and Tcf4 depletion from intestinal epithelial cells is accomplished by administration of tamoxifen. After 7 days, small red structures, i.e. \\"escaped crypts\\", appear in the epithelium, marking proliferative zones that appear to have escaped Tcf4 deletion. We performed gene expression profiling of RFP+ cells from these \\"escaped crypts\\" and from crypts isolated from wild-type epithelium.

2026-06-29 | E-MTAB-13731 | biostudies-arrayexpress

UBC9 knockdown in bladder cancer T24 cell lines

Project description:UBC9 is the sole conjugating enzyme E2 in the sumoylation and plays a pivotal role in maintaining homeostasis and restraining stress reaction. Targeting UBC9 is emerging as a novel strategy for cancer therapy. However, the role of UBC9 in bladder cancer is not clear. Here, we sought to determine the alterations of trancriptome after shRNA-mediated knockdown UBC9 in T24 cell lines．

2018-12-25 | GSE117143 | GEO

scRNA-seq of Bcl9/9l fl/fl;Rosa26-CreERT2 small intestinal organoids

Project description:Bcl9/9l fl/fl;Rosa26-CreERT2 small intestinal organoids were exposed to 1uM 4-OHT (or EtOH as a control) for 24 hours to induce recombination and induce a conditional Bcl9 and Bcl9l knockout. Intestinal epithelial cells were isolated 72 hours later for single cell RNA sequencing. BCL9 is a beta-catenin transcriptional cofactor involved in the transcriptional machinery of Wnt target genes. We found that BCL9/9L is a key player in coordinating the balance between Wnt mediated proliferation and differentiation in the intestinal epithelium by engaging with GATA transcription factors. In line with this observation, we observed an increase in secretory lineage cells upon loss of Bcl9/9l in intestinal organoids.

2026-07-07 | E-MTAB-16966 | biostudies-arrayexpress

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