Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: ZP1 RNA&Pro

PROVIDER: PRJNA1273651 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR33884423_1.fastq.gz	Fastqsanger.gz
	SRR33884423_2.fastq.gz	Fastqsanger.gz
	SRR33884424_1.fastq.gz	Fastqsanger.gz
	SRR33884424_2.fastq.gz	Fastqsanger.gz
	SRR33884425_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 28

Similar Datasets

HeberleRazquinNavas2019 - The PI3K and MAPK/p38 pathways control stress granuleassembly in a hierarchical manner model 3

Project description:All cells and organisms exhibit stress-coping mechanisms toensure survival. Cytoplasmic protein-RNA assemblies termedstress granules are increasingly recognized to promote cellularsurvival under stress. Thus, they might represent tumor vul-nerabilities that are currently poorly explored. The translation-inhibitory eIF2αkinases are established as main drivers ofstress granule assembly. Using a systems approach, we identifythe translation enhancers PI3K and MAPK/p38 as pro-stress-granule-kinases. They act through the metabolic master regu-lator mammalian target of rapamycin complex 1 (mTORC1) topromote stress granule assembly. When highly active, PI3K is themain driver of stress granules; however, the impact of p38becomes apparent as PI3K activity declines. PI3K and p38 thusact in a hierarchical manner to drive mTORC1 activity and stressgranule assembly. Of note, this signaling hierarchy is also presentin human breast cancer tissue. Importantly, only the recognition ofthe PI3K-p38 hierarchy under stress enabled the discovery of p38’srole in stress granule formation. In summary, we assign a new pro-survival function to the key oncogenic kinases PI3K and p38, as theyhierarchically promote stress granule formation

2024-09-02 | BIOMD0000000907 | BioModels

HeberleRazquinNavas2019 - The PI3K and MAPK/p38 pathways control stress granuleassembly in a hierarchical manner model 2

Project description:All cells and organisms exhibit stress-coping mechanisms to ensure survival. Cytoplasmic protein-RNA assemblies termed stress granules are increasingly recognized to promote cellular survival under stress. Thus, they might represent tumor vulnerabilities that are currently poorly explored. The translation-inhibitory eIF2α kinases are established as main drivers of stress granule assembly. Using a systems approach, we identify the translation enhancers PI3K and MAPK/p38 as pro-stress-granule-kinases. They act through the metabolic master regulator mammalian target of rapamycin complex 1 (mTORC1) to promote stress granule assembly. When highly active, PI3K is the main driver of stress granules; however, the impact of p38 becomes apparent as PI3K activity declines. PI3K and p38 thus act in a hierarchical manner to drive mTORC1 activity and stress granule assembly. Of note, this signaling hierarchy is also present in human breast cancer tissue. Importantly, only the recognition of the PI3K-p38 hierarchy under stress enabled the discovery of p38’s role in stress granule formation. In summary, we assign a new pro-survival function to the key oncogenic kinases PI3K and p38, as they hierarchically promote stress granule formation.

2024-09-26 | MODEL2001030002 | BioModels

Brg1 activates enhancer repertoires to establish B cell identity and modulate cell growth

Project description:Early B cell development is orchestrated by the combined activities of the transcriptional regulators E2A, EBF1, Foxo1 and Ikaros. However, how the genome-wide binding patterns of these regulators are modulated during B-lineage development remains to be determined. Here, we found that in lymphoid progenitors the chromatin remodeler Brg1 specified the B cell fate. In committed pro-B cells Brg1 regulated Igh locus contraction and controlled c-Myc expression to modulate the expression of genes that regulate ribosome biogenesis. In committed pro-B cells Brg1 also suppressed a pre-B lineage-specific pattern of gene expression. Finally, we found that Brg1 acted mechanistically to establish B cell fate and modulate cell growth by facilitating access of lineage-specific transcription factors to poised enhancer repertoires. 8 ATAC-Seq samples from sorted ALP and BLP (duplicates, control and Brg1-deleted), 4 ATAC-Seq samples from cultured pro-B cells (duplicates, control and Brg1-deleted), 2 Ikaros ChIP-seq samples (performed in Rag1-/- pro-B cells and in E2A-/- pre-pro-B cells), 1 Brg1 ChIP-seq sample and accompanying Input sample (both in Rag1-/- pro-B cells), 4 RNA-Seq samples from cultured pro-B cells (duplicates, control and Brg1-deleted), 6 RNA-Seq samples from cultured Rag1-/- pro-B cells (triplicates, control and Brg1-knock down).

2015-05-15 | E-GEOD-66978 | biostudies-arrayexpress

Microprotein-Encoding RNA Regulation in Cells Treated with Pro-inflammatory and Pro-Fibrotic Stimuli (RNA-Seq Caco2)

Project description:Microprotein-Encoding RNA Regulation in Cells Treated with Pro-inflammatory and Pro-Fibrotic Stimuli (RNA-Seq Caco2)

| PRJNA1121292 | ENA

Microprotein-Encoding RNA Regulation in Cells Treated with Pro-inflammatory and Pro-Fibrotic Stimuli

Project description:Microprotein-Encoding RNA Regulation in Cells Treated with Pro-inflammatory and Pro-Fibrotic Stimuli

| PRJNA1121277 | ENA

Microprotein-Encoding RNA Regulation in Cells Treated with Pro-inflammatory and Pro-Fibrotic Stimuli (RNA-Seq colon cell lines)

Project description:Microprotein-Encoding RNA Regulation in Cells Treated with Pro-inflammatory and Pro-Fibrotic Stimuli (RNA-Seq colon cell lines)

| PRJNA1121291 | ENA

RNA-seq of Tnpo3fl/fl pro-B cells

Project description:RNA-seq of Tnpo3fl/fl pro-B cells

| PRJNA832133 | ENA

Improving Adolescent and Young Adult Self-Reported Data in ECOG-ACRIN Trials

Project description:The purpose of this study is to evaluate feasibility and acceptability of completing PROs among AYAs randomized to Choice PRO vs Fixed PRO.

| 2394564 | ecrin-mdr-crc

The B cell identity factor Pax5 regulates distinct transcriptional programs in early and late B lymphopoiesis

Project description:Pax5 controls the identity and development of B cells by repressing lineage-inappropriate genes and activating B-cell-specific genes. Here, we used genome-wide approaches to identify Pax5 target genes in pro-B and mature B cells. In these cell types, Pax5 bound to 40% of the cis- regulatory elements defined by mapping Dnase I hypersensitive (DHS) sites, transcription start sites and histone modifications. Although Pax5 bound to 8,000 target genes, it regulated only 4% of them in pro-B and mature B cells by inducing enhancers at activated genes and eliminating DHS sites at repressed genes. Pax5-regulated genes in pro-B cells account for 23% of all expression changes occurring between common lymphoid progenitors and committed pro-B cells, which identifies Pax5 as an important regulator of this developmental transition. Regulated Pax5 target genes minimally overlap in pro-B and mature B cells, which reflects massive expression changes between these cell types. Hence, Pax5 controls B cell identity and function by regulating distinct target genes in early and late B lymphopoiesis. 44 samples (16 RNA-seq, 15 ChIP-seq, 6 DHS-seq, 5 Bio-ChIP-seq, 2 CAGE-seq). All but four samples in in 2 biological replicates (8819, 8275, 8095, 8666). WT and experimental samples are provided.

2012-06-14 | E-GEOD-38046 | biostudies-arrayexpress

Evaluating the Use of Patient-Reported Outcome Measures for Improving the Inter-Rater Reliability of Common Terminology Criteria for Adverse Event Ratings

Project description:This open randomized trial investigates, if clinicians complete CTCAE ratings differently when receiving patients’ patient-reported outcome (PRO) data prior to their CTCAE completion. The primary objective is to demonstrate superior inter-rater reliability of CTCAE ratings from physicians relying on EORTC PRO data as additional data source over traditional CTCAE ratings not including PRO information.

| 2314534 | ecrin-mdr-crc

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