Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE196916 | GEO | 2023/04/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse [scRNA-seq]

Project description:The goal of this study is to survey transcriptional machinery in intestinal stem cells from small and large intestine of mice. We established intestinal stem cell specific gene-regulatroy network to understand regional identity.

2023-04-20 | GSE196915 | GEO

Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse [RNA-seq]

2023-04-20 | GSE196914 | GEO

Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse [ATAC-seq]

2023-04-20 | GSE196913 | GEO

Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse

Project description:Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse

| PRJNA807704 | ENA

Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse [scRNA-seq]

Project description:Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse [scRNA-seq]

| PRJNA807706 | ENA

Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse [ATAC-seq]

Project description:Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse [ATAC-seq]

| PRJNA807708 | ENA

Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse [RNA-seq]

Project description:Generation of transcriptional regulatory network of Lgr5+ small and large intestinal stem cells from mouse [RNA-seq]

| PRJNA807707 | ENA

Vitamin D is a determinant of mouse intestinal Lgr5 stem cell functions.

Project description:Lgr5+ intestinal crypt base columnar cells function as stem cells whose progeny populate the villi, and Lgr5+ cells in which Apc is inactivated can give rise to tumors. Surprisingly, these Lgr5+ stem cell properties were abrogated by the lower dietary vitamin D and calcium in a semi-purified diet that promotes both genetically initiated and sporadic intestinal tumors. Inactivation of the vitamin D receptor in Lgr5+ cells established that compromise of Lgr5 stem cell function was a rapid, cell autonomous effect of signaling through the vitamin D receptor. The loss of Lgr5 stem cell function was associated with presence of Ki67 negative Lgr5+ cells at the crypt base. Therefore, vitamin D, a common nutrient and inducer of intestinal cell maturation, is an environmental factor that is a determinant of Lgr5+ stem cell functions in vivo. Since diets used in reports that establish and dissect mouse Lgr5+ stem cell activity likely provided vitamin D levels well above the range documented for human populations, the contribution of Lgr5+ cells to intestinal homeostasis and tumor formation in humans may be significantly more limited, and variable in the population, then suggested by published rodent studies.

| S-EPMC4303796 | biostudies-literature

LGR5+ Intestinal Stem Cells Display Sex-Dependent Radiosensitivity.

Project description:Tissue radiosensitivity plays a critical role in the overall outcome of radiation therapy. Identifying characteristics that predict how a patient may respond to radiotherapy enables clinicians to maximize the therapeutic window. Limited clinical data have suggested a difference in male and female radiotherapy outcomes. Radiotherapy for gastrointestinal malignancy is still a challenge due to intestinal sensitivity to radiation toxicity. In this manuscript, we demonstrated sex-specific differences in intestinal epithelial radiosensitivity. In a mouse model of abdominal irradiation, we observed a significant increase in oxidative stress and injury in males compared to females. Lgr5+ve intestinal stem cells from male mice showed higher sensitivity to radiation-induced toxicity. However, sex-specific differences in intestinal radiosensitivity were not dependent on sex hormones, as we demonstrated similar sex-specific radiosensitivity differences in pre-pubescent mice. In an ex vivo study, we found that patient-derived intestinal organoid (PID) from males showed higher sensitivity to radiation compared to females as evident from loss of budding crypts, organoid size, and membrane integrity. Transcriptomic analysis of human Lgr5+ intestinal stem cells suggested radiation-induced upregulation of mitochondrial oxidative metabolism in males compared to females, a possible mechanism for radiosensitivity differences.

| S-EPMC10778194 | biostudies-literature

YY1 is indispensable for Lgr5+ intestinal stem cell renewal.

Project description:The intestinal stem cell fuels the highest rate of tissue turnover in the body and has been implicated in intestinal disease and cancer; understanding the regulatory mechanisms controlling intestinal stem cell physiology is of great importance. Here, we provide evidence that the transcription factor YY1 is essential for intestinal stem cell renewal. We observe that YY1 loss skews normal homeostatic cell turnover, with an increase in proliferating crypt cells and a decrease in their differentiated villous progeny. Increased crypt cell numbers come at the expense of Lgr5(+) stem cells. On YY1 deletion, Lgr5(+) cells accelerate their commitment to the differentiated population, exhibit increased levels of apoptosis, and fail to maintain stem cell renewal. Loss of Yy1 in the intestine is ultimately fatal. Mechanistically, YY1 seems to play a role in stem cell energy metabolism, with mitochondrial complex I genes bound directly by YY1 and their transcript levels decreasing on YY1 loss. These unappreciated YY1 functions broaden our understanding of metabolic regulation in intestinal stem cell homeostasis.

| S-EPMC4040551 | biostudies-literature

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