Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Atf4 promotes erythroid differentiation by regulating ribosome biogenesis via RPS19BP1

ABSTRACT: To elucidate the mechanisms underlying the role of Atf4 deficiency in erythropoiesis, we performed 10X Genomics single-cell RNA sequencing on Lin-cKit+ cells from Atf4 hematopoietic cell-specific conditional knockout mice (KO) and Atf4 floxed mice (WT) at steady state (referred to KO_BM and WT_BM) and after secondary transplantation (referred to cKO_t and WT_t). Furthermore, we also sorted CMP cells from Atf4 hematopoietic cell-specific conditional knockout mice (KO) and ATF4 floxed mice (WT) for 10X Genomics scRNA-seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE235798 | GEO | 2024/03/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression data of LT-HSC, MEP and CMP cells from Mx1cre;Atf4 fl/fl mice(cKO) BM and those from controls

Project description:To elucidate the mechanisms underlying the role of Atf4 deficiency in erythropoiesis, we performed RNA sequencing on LT-HSC, MEP and CMP cells from Atf4 hematopoietic cell-specific conditional knockout mice(cKO) and those from WT mice.

2024-03-15 | GSE233677 | GEO

Effect of bone marrow-specific aryl hydrocarbon receptor (Ahr) gene knockout on expression profiles of hematopoietic stem cells from young and old mice.

Project description:As part of a study of the role of the aryl hydrocarbon receptor (Ahr) in maintenance and senescence of hematopoietic stem cells (HSC), global gene expression profiling was done with HSC isolated from bone marrow restricted conditional Ahr-knockout and AhR floxed mice. HSC from young-adult (8 wk old) cAhR-KO mice had changes in expression of many genes related to HSC maintenance, consistent with the phenotype observed in Ahr-KO mice. Aged cAhR-KO mice (18 months old) also displayed alterations in peripheral white blood cell counts, serial repopulation potential and levels of ROS in bone marrow cells, consistent with previous observations on the role of AhR in the hematopoietic system. 22 samples: 5 young Ahr knockout, 6 old Ahr knockout, 5 young floxed Ahr, 6 old floxed Ahr

2016-06-30 | E-GEOD-76276 | biostudies-arrayexpress

Ets1 dampens expression of Tbet and CD8- or NK-like effector programing in postselection iNKT1 cells [scRNA-seq]

Project description:The goal of this study was to compare the gene expression program of thymic iNKT1 cells from Control mice to those with a postselection deletion of the transcription factor Ets1 at the single cell level. Ets1-floxed alleles were deleted in iNKT1 cells using Tbx21Cre bacterial artifical chromosome transgenic mice that also carry a Rosa26-floxed-stop-YFP reporter. Control iNKT1 cells were Tbx21Cre+ Rosa26-floxed-stop-YFP reporter+. We isolated all thymic YFP+ cells from Control and cKO mice and processed for scRNA-seq using the 10X Genomics Chromium. Data was processed using the Cell Ranger program for 10X Genomics. . We found that iNKT1 cells lacking Ets1 upregulated Tbx21 and its protein Tbet, many Tbet target genes, and CD8 effector T cell associated genes.

2024-10-10 | GSE278707 | GEO

Effect of bone marrow-specific aryl hydrocarbon receptor (Ahr) gene knockout on expression profiles of hematopoietic stem cells from young and old mice.

2016-06-30 | GSE76276 | GEO

Trib1 regulates T cell differentiation during chronic infection by restraining the effector program

Project description:Using the 10X Genomics platform, we performed single cell RNA-sequencing on activated T cells from LCMV clone 13-infected control or CD4-cre+ Trib1-floxed mice to determine how Trib1 regulates T cell population dynamics during chronic infection.

2020-03-05 | GSE143802 | GEO

Expression data from Foxl2 wild-type and mutant ovaries and testes

Project description:Foxl2 is a forkhead transcription factor expressed only in the female, but not in the male gonad. We have created mice homozygous mutant for the Foxl2 gene (KO) as well as mice carrying a conditional mutant Foxl2 allele (floxed). The expression profiles of conventional Foxl2 knockout and wildtype ovaries were compared at P3, using the Affy Mouse Genome 430 2.0 Array. Adult wildtype and conditional mutant (Foxl2 floxed x RosaCre-EBD treated with tamoxifen) ovaries were compared to adult wildtype testes using the Affymetrix Mouse Gene 1.0 ST Array. Both experiments (KO/WT P3 and Mutant/WT/Testis Adult were also compared to each other.)

2010-01-01 | GSE16853 | GEO

LKB1 and Notch deletion in mouse liver

Project description:We characterize the phenotype of mice in which the deletion of Lkb1 has been targeted in the liver. Lack of Lkb1 in the liver results in bile duct paucity leading to cholestasis. This phenotype is similar to that obtained upon inactivation of Notch signaling in the liver. We test the hypothesis of a functional overlap between the Lkb1 and Notch pathways by gene expression profiling of livers deficent in Lkb1 or in the Notch mediator RbpJÎº. We used AlfpCre mice for liver-specific deletion of LKB1 that were crossed with a conditional knockout mouse model (LKB1 floxed mice). We used also AlfpCre mice for liver-specific inactivation of the Notch pathway. AlfpCre mice were crossed with the RbpJÎº floxed mice. RNA was extracted from the liver of LKB1 KO mice (Lkb1Floxed, AlfpCre positive mice) and their wild-type counterpart (Lkb1Floxed, AlfpCre negative mice). RNA was also extracted from liver of RbpJK KO mice (RbpJK floxed, AlfpCre positive) and their wild type mice (RbpJK floxed, AlfpCe negative). 6 samples for the liver-specific deletion of LKB1 corresponding to 3 KO LKB1 (Cre positive) and 3 normal liver (Cre negative). 6 samples for the liver-specific inactivation of the Notch pathway corresponding to 3 KO RbpJk (Cre positive) and 3 normal liver (Cre negative).

2015-12-08 | E-GEOD-75564 | biostudies-arrayexpress

Single-cell RNA-seq on enriched cardiac fibroblasts from the healthy, sham or MI hearts of Hif-1a conditional knockout or heterozygous mice

Project description:In this project we explore the role of the master hypoxia regulator, Hypoxia inducible factor-1alpha (Hif-1a), in governing cardiac fibroblast (CF) function in homeostasis and following an acute ischaemic injury - myocardial infarction (MI). CF-specific Hif-1a conditional knockout (cKO) mice were generated by breeding Pdgfra-merCremer (PdgfraMCM/+) Cre recombinase driver mice with Hif-1a-floxed mice (Hif-1aflox/). In Hif-1afl/-; PdgfraMCM/+ progeny, Hif-1a could be conditionally deleted in adult CFs by tamoxifen (tam) administration. We also introduced a Cre-dependent R26tdTomato reporter allele allowing marking of Pdgfra+ CFs and their progeny. In this experiment, we first performed single-cell RNA sequencing (scRNA-seq) on tdTomato+ cells from the hearts of healthy cKO or heterozygous (HET) adult, male mice using the 10x Genomics Chromium system. We also performed scRNA-seq on tdTomato+/CD31-/CD45- cells from the hearts of cKO or HET mice at day-3 post-sham or -MI surgery.

2021-11-11 | E-MTAB-9583 | biostudies-arrayexpress

Single Cell Profiling of DNMT3A-Mutant Progenitors Novel Pre-Leukemia Marker and Potential Therapeutic Target

Project description:To identify early events involved in pre-leukemic transformation, we have performed single-cell RNA-sequencing (scRNA-seq) in WT and Dnmt3a KO mice. Flow cytometry sorted wild-type and pre-leukemic Dnmt3a KO HSPC cells were captured using 10X genomics chromium platform.

2021-12-01 | GSE154624 | GEO

LKB1 and Notch deletion in mouse liver

Project description:We characterize the phenotype of mice in which the deletion of Lkb1 has been targeted in the liver. Lack of Lkb1 in the liver results in bile duct paucity leading to cholestasis. This phenotype is similar to that obtained upon inactivation of Notch signaling in the liver. We test the hypothesis of a functional overlap between the Lkb1 and Notch pathways by gene expression profiling of livers deficent in Lkb1 or in the Notch mediator RbpJκ. We used AlfpCre mice for liver-specific deletion of LKB1 that were crossed with a conditional knockout mouse model (LKB1 floxed mice). We used also AlfpCre mice for liver-specific inactivation of the Notch pathway. AlfpCre mice were crossed with the RbpJκ floxed mice. RNA was extracted from the liver of LKB1 KO mice (Lkb1Floxed, AlfpCre positive mice) and their wild-type counterpart (Lkb1Floxed, AlfpCre negative mice). RNA was also extracted from liver of RbpJK KO mice (RbpJK floxed, AlfpCre positive) and their wild type mice (RbpJK floxed, AlfpCe negative).

2015-12-08 | GSE75564 | 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