Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

14 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq on hematopoietic stem cells sorted from mice 1 month after they were irradiated (2Gy total body irradiation = IR) or not (non irradiated = NIR) and with or without prior TNFa treatment (IR_TNF)

ABSTRACT: Analysis of the RNA-seq data performed in IR vs NIR hematopoietic stem cells show the loss of the TNF_via_NFKB signature. We showed that the loss of this signature could be associated with hematopoietic stem cell gene deregulation. To validate this association, we tested if TNFa treatment before irradiation was able to prevent IR-effect on HSC gene deregulation. For this purpose, we treated mice with TNFa 1h before irradiation (IR_TNF) and performed RNA-seq experiments on hematopoietic stem cells 1 month after irradiation and compared them to hematopoietic stem cells sorted from non irradiated mice (NIR) and from non-treated irradiated mice (IR).

ORGANISM(S): Mus musculus

SUBMITTER: Emilie Elvira-Matelot

PROVIDER: E-MTAB-11867 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

H3K9me3 Cut&Tag on hematopoietic stem cells sorted from mice 1 month after they were irradiated (2Gy total body irradiation = IR) or not (non irradiated = NIR) and with or without prior TNFa treatment (IR_TNF)

Project description:Analysis of the RNA-seq data performed in IR vs NIR hematopoietic stem cells show the loss of the TNF_via_NFKB signature. We showed that the loss of this signature could be associated with H3K9me3 loss at specific retrotransposable elements . To validate this association, we tested if TNFa treatment before irradiation was able to prevent IR-effect on H3K9me3 loss at retrotransposable elements. For this purpose, we treated mice with TNFa 1h before irradiation (IR_TNF) and performed H3K9me3 cut&tag experiments on hematopoietic stem cells 1 month after irradiation and compared them to hematopoietic stem cells sorted from non irradiated mice (NIR) and from non-treated irradiated mice (IR).

2022-06-24 | E-MTAB-11864 | biostudies-arrayexpress

H3K9me3 ChIP-seq on hematopoietic stem cells sorted from mice 1 month after they were irradiated (2Gy total body irradiation = IR) or not (non irradiated = NIR)

Project description:We aim at understanding how ionizing radiations (IR) increase the risk of developing myeloid leukemia. We recently showed that IR leads to the derepression of retroelements. We demonstrated that retroelements expression in aged HSCs is regulated by the heterochromatin repressive histone mark H3K9me3. However, the mechanisms by which IR specifically triggers retroelements expression in HSCs are unknown. We hypothesized that retroelements derepression is due to IR-induced heterochromatin changes. To answer this question, we performed H3K9me3 ChIP-seq experiments in hematopoietic stem cells sorted from mice one month after they were irradiated and compared them to controls hematopoietic stem cells sorted from non-irradiated mice.

2022-06-24 | E-MTAB-11865 | biostudies-arrayexpress

RNA-seq on hematopoietic stem cells sorted from mice 1 month after they were irradiated (2Gy total body irradiation = IR) or not (non irradiated = NIR)

Project description:We aim at understanding how ionizing radiations (IR) increase the risk of developing myeloid leukemia. We recently showed that IR leads to the derepression of retroelements. Retroelements are major contributors of gene regulatory networks. However, the impact of retroelements derepression on the HSC transcriptome and function remains to be addressed. We hypothesized that retroelements derepression is involved in HSC transcriptomic alterations. To answer this question, we performed RNA-seq experiments in hematopoietic stem cells sorted from mice one month after they were irradiated and compared them to controls hematopoietic stem cells sorted from non-irradiated mice.

2022-06-24 | E-MTAB-11866 | biostudies-arrayexpress

RNA-seq on hematopoietic stem cells sorted from mice 1 month after they were irradiated (2Gy total body irradiation = IR) or not (non irradiated = NIR)

Project description:RNA-seq on hematopoietic stem cells sorted from mice 1 month after they were irradiated (2Gy total body irradiation = IR) or not (non irradiated = NIR)

| PRJEB53833 | ENA

H3K9me3 ChIP-seq on hematopoietic stem cells sorted from mice 1 month after they were irradiated (2Gy total body irradiation = IR) or not (non irradiated = NIR)

Project description:H3K9me3 ChIP-seq on hematopoietic stem cells sorted from mice 1 month after they were irradiated (2Gy total body irradiation = IR) or not (non irradiated = NIR)

| PRJEB53831 | ENA

RNA-seq on hematopoietic stem cells sorted from mice 1 month after they were irradiated (2Gy total body irradiation = IR) or not (non irradiated = NIR) and with or without prior TNFa treatment (IR_TNF)

Project description:RNA-seq on hematopoietic stem cells sorted from mice 1 month after they were irradiated (2Gy total body irradiation = IR) or not (non irradiated = NIR) and with or without prior TNFa treatment (IR_TNF)

| PRJEB53832 | ENA

Project description:H3K9me3 Cut&Tag on hematopoietic stem cells sorted from mice 1 month after they were irradiated (2Gy total body irradiation = IR) or not (non irradiated = NIR) and with or without prior TNFa treatment (IR_TNF)

| PRJEB53827 | ENA

E-MTAB-11867

2023-06-15 | E-MTAB-11867 | ExpressionAtlas

E-MTAB-11866

Project description:RNA-seq on hematopoietic stem cells sorted from mice 1 month after they were irradiated (2Gy total body irradiation = IR) or not (non irradiated = NIR)

2023-06-15 | E-MTAB-11866 | ExpressionAtlas

Global Phosphoproteomics of BRCA1-deficient mammary tumors in genetic mouse models

Project description:The aim of the study is to identify differences in the global phosphoproteome across a BRCA1-deficient mouse mammary tumor panel. We have matched PARPi-naive and PARPi-resistant tumors, in which resistance was induced in vivo (mice bearing tumors were treated with PARPi untill the tumors stopped responding). Each pair of matched naive/resistant tumors originate from a different original tumor donor (one can consider each individual donor as an individual patient). From another analysis (RAD51 IRIF) we know that the mechanism of PARPi-resistance in a number of the tumors is driven by alterations in DNA damage response. Therefore, we can divide the tumors into four groups: (A) HR proficient, the exact mechanism not known, (B) HR proficient due to the loss of 53bp1 (TP53BP1), (C) HR proficient due to loss of Rev7 (MAD2L2) and (D) HR deficient, mechanism of resistance not known. Additionally, each tumor from our panel was retransplanted and challenged with 15 Gy irradiation to trigger a DNA damage response, therefore for each tumor we have an irradiated (IR) and a non-irradiated (NIR) sample. In this experiment each sample was processed in duplicate. Given all this, group (A) consists of 6 individual donors x 2 (matched naive/resistant) x 2 (NIR/IR) x 2 (duplicate) = 48 samples (samples 1-48); groups (B)-(D): 2 donors (per group) x 2 (naive/resistant) x 2 (NIR/IR) x 2 (duplicate) = 16 samples/group (B: samples 65-80, C: samples 81-96 and D: 49-64, according to the OPL label). In total this gives: 48 + 16 +16 +16 = 96 samples. Part of this analysis is used in the paper that also describes data from PXD031711

2022-06-06 | PXD032007 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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