Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene profile beween CD19 normal and deletion of resting B cells in spleen of sirt1 conditional knockout mouse

ABSTRACT: Gene profile beween CD19 normal and deletion of resting B cells in spleen of sirt1 conditional knockout mouse

PROVIDER: PRJNA496623 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Gene profile beween CD19 normal and deletion of resting B cells in spleen of sirt1 conditional knockout mouse

Project description:Gene profile beween CD19 normal and deletion of resting B cells in spleen of sirt1 conditional knockout mouse

2019-05-01 | GSE121306 | GEO

RNAseq in Sirt1 wild-type or conditional KO mouse T-ALLs

Project description:C57BL6 mice harboring Sirt1 conditional knockout NOTCH1-DE-induced leukemias were treated with vehicle (control) or tamoxifen to induce isogenic deletion of Sirt1. Here we report the gene expression profile of leukemic blasts obtained from the spleen from control- or tamoxifen-treated leukemic mice.

2022-12-08 | GSE203387 | GEO

Gene expression profiling of spleen marginal zone B cells and spleen follicular B cells in IRF8 conditional KO mice

2010-12-20 | GSE24972 | GEO

Gene expression profiling of spleen marginal zone B cells and spleen follicular B cells in IRF8 conditional KO mice

Project description:Conditional IRF8 KO mice (mice with a conditional allele of Irf8 crossed with CD19-Cre mice) showed increased numbers of both Gene expression data spleen marginal zone (MZ) and Gene expression data spleen follicular (FO) B cells compared to control mice. To evaluate gene expression patterns that distinguished FO or MZ B cells derived from conditional KO and control mice, we used Affymetrix GeneChip® Mouse gene 1.0 ST Array. FACS-sorted MZ and FO B cells from individual mouse were used for RNA extraction and Affyarray hybridization. There were six independent biological replications in each group - six cases of MZ B cells and FO cells in IRF8 conditional KO mice and six cases of MZ B cells and FO cells in control WT mice.

2010-12-20 | E-GEOD-24972 | biostudies-arrayexpress

RNAseq in Sirt1 wild-type or deleted mouse T-ALLs

Project description:C57BL6 mice harboring Sirt1 conditional knockout NOTCH1-HDDPEST-induced leukemias were treated with vehicle (control) or tamoxifen to induce isogenic deletion of Sirt1. Here we report the gene expression profile of leukemic blasts obtained from the spleen from control- or tamoxifen-treated leukemic mice.

2024-01-01 | GSE192842 | GEO

A therapeutically targetable NOTCH1-SIRT1-KAT7 axis in T-ALL

Project description:C57BL6 mice harboring Sirt1 conditional knockout NOTCH1-DE-induced leukemias were treated with vehicle (control) or tamoxifen to induce isogenic deletion of Sirt1. Here we report the H4K12ac ChIP-seq epigenetic profile of leukemic blasts obtained from the spleen from control- or tamoxifen-treated leukemic mice.

2022-12-08 | GSE203386 | GEO

Gene expression of resting memory, resting naive and in vitro activated memory CD8+CD127+ T cells from spleen and bone marrow (BM)

Project description:To understand differences between resting and activated memory CD8+ T cells, we compared the global gene expression of ex vivo isolated naive and spleen and BM memory cells to in vitro activated spleen and BM memory cells.

2015-02-05 | GSE62691 | GEO

RNAseq in Sirt1 wild-type or conditional KO mouse T-ALLs

Project description:RNAseq in Sirt1 wild-type or conditional KO mouse T-ALLs

| PRJNA839727 | ENA

RNA-Seq profiling of Sirt1 deficient mouse oocytes to investigate Sirt1 role in maternal-zygotic transition

Project description:Sirtuin-1 (Sirt1), a NAD+-dependent histone deacetylase, exhibits several properties of a versatile driver of maternal-zygotic transition, due to its epigenetic and non-epigenetic substrates. The study was aimed at the dynamics of Sirt1 in early embryos and the contribution to maternal-zygotic transition. A conditional Sirt1-deficient knock-out mouse model was used. Females were hormonally stimulated and used as oocyte donors. oocytes were parthenogenetically activated and Sirt1-/- two-cell embryos were used for transcriptomic analysis.

2024-07-06 | E-MTAB-13483 | biostudies-arrayexpress

SIRT1 negatively regulates the differentiation of IL-9-producing CD4+T cells

Project description:Distinct metabolic programs support the differentiation of CD4+T cells into their separate lineages. In this study, we investigated metabolic mechanisms underlying the differentiation of IL-9 producing-CD4+T cells (TH9) in allergic airway inflammation and cancerous tumors. We found here that SIRT1 negatively regulates TH9 differentiation. A deficiency of SIRT1 induced by either conditional deletion in mouse CD4+T cells or the use of small interfering RNA (siRNA) in mouse or human T cells increased IL-9 production, whereas ectopic SIRT1 expression inhibited it. Notably, SIRT1-inhibited the differentiation of TH9 cells that regulated anti-tumor immunity and allergic pulmonary inflammation. Glycolytic activation through the mTOR-hypoxia-inducible factor-1Î± (HIF1Î±) pathway was required for the differentiation of the TH9 cells that confer protection against tumors and are involved in allergic airway inflammation. Our results define the essential features of a SIRT1-mTOR-HIF1Î± signaling-coupled glycolytic pathway in inducing TH9 cell differentiation, with implications for metabolic reprogramming as an immunotherapeutic approach. Lymphocytes were isolated from the spleen and lymph nodes of mice and sorted on a FACSAria II (Becton Dickinson). The sorted naÃ¯ve T cells (CD4+TCR+CD62Lhi CD44lo) from WT or SIRT1flox/flox-CD4-Cre mice were used for in vitro culture. T cells were activated with 2 ug/ml anti-CD3 (2C11; Bio X Cell), 2 ug/ml anti-CD28 (37.51; Bio X Cell) and 100 U/ml human IL-2. For TH9 cell differentiation, cultures were supplemented with 10 ng/ml IL-4 (R&D system), 2 ng/ml TGFÎ²1 (R&D system). After 5-6 d culture, differentiated T cells were collected and for microarray assay.

2016-06-14 | E-GEOD-79607 | 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