Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A global wiring diagram of stress response signaling

ABSTRACT: A global wiring diagram of stress response signaling

PROVIDER: PRJNA475469 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR7287620.fastq.gz	Fastqsanger.gz
	SRR7287630.fastq.gz	Fastqsanger.gz
	SRR7287640.fastq.gz	Fastqsanger.gz
	SRR7287650.fastq.gz	Fastqsanger.gz
	SRR7287660.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 391

Similar Datasets

A global wiring diagram of stress response signaling

Project description:We perform RNA-seq on 28 analog sensitive kinase alleles across 12 different conditions. We use this to determine condition specific kinase function on the transcriptional response.

2019-02-08 | GSE115556 | GEO

A global timing mechanism regulates cell-type specific wiring programs

Project description:The assembly of neural circuits is dependent upon precise spatiotemporal expression of cell recognition molecules1–6. Factors controlling cell-type specificity have been identified7–9, but how timing is determined remains unknown. Here we describe the induction of a cascade of transcription factors by a steroid hormone (Ecdysone) in all fly visual system neurons spanning target recognition and synaptogenesis. We demonstrate through single cell sequencing that the Ecdysone pathway regulates the expression of a common set of targets required for synaptic maturation and cell-type specific targets enriched for cell surface proteins regulating wiring specificity. Transcription factors in the cascade regulate the expression of the same wiring genes in complex ways, including activation in one cell-type and repression in another. We show that disruption of the Ecdysone-pathway generates specific defects in dendritic and axonal processes and synaptic connectivity, with the order of transcription factor expression correlating with sequential steps in wiring. We also identify shared targets of a cell-type specific transcription factor and the Ecdysone pathway which regulate specificity. We propose neurons integrate a global temporal transcriptional module with cell-type specific transcription factors to generate different cell-type specific patterns of cell recognition molecules regulating wiring.

2021-12-14 | GSE190714 | GEO

A global timing mechanism regulates cell-type specific wiring programs

Project description:A global timing mechanism regulates cell-type specific wiring programs

| PRJNA788151 | ENA

Cue-induced modulation of eIF2α-eIF2Bε underlies axonal translation up-regulation in neural wiring

Project description:Local protein synthesis is rapidly regulated by extrinsic signals during neural wiring but the translational control mechanisms remain elusive. Here, we show that the guidance cue Sema3A, but not Slit1, elicits precise spatiotemporal control of the phosphorylation of the translation initiation factor, eIF2α, in axonal growth cones via the Unfolded Protein Response (UPR) kinase PERK. Strikingly, in contrast to the canonical UPR signaling, we find that the Sema3A-induced eIF2α phosphorylation bypasses the conventional global translational repression and underlies a burst in axonal protein synthesis, mediated by differential eIF2B activity. Ultrasensitive proteomics on somaless axons reveals a subset of 75 proteins translationally regulated via Sema3A-p-eIF2α, including several proteostasis- and actin cytoskeleton-related nascent proteins. Finally, in vivo experiments provide evidence that eIF2α phosphorylation drives the formation of the retinotectal axon projection. Thus, specific extracellular cues can trigger non-canonical PERK-eIF2α-eIF2B signaling leading to subcellular dynamic remodeling of the nascent proteome required for neural wiring.

2019-01-02 | PXD009250 | Pride

Dynamic re-wiring of apoptotic signaling networks enhances tumor cell killing by DNA damage

Project description:Crosstalk and complexity within signaling pathways has limited our ability to devise rational strategies for using network biology to treat human disease. This is particularly problematic in cancer where oncogenes that drive or maintain the tumorigenic state alter the normal flow of molecular information within signaling networks that control growth, survival and death. Understanding the architecture of oncogenic signaling pathways, and how these networks are re-wired by ligands or drugs, could provide opportunities for the specific targeting of oncogene-driven tumors. Here we use a systems biology-based approach to explore synergistic therapeutic strategies to optimize the killing of triple negative breast cancer cells, an incompletely understood tumor type with a poor treatment outcome. Using targeted inhibition of oncogenic signaling pathways combined with DNA damaging chemotherapy, we report the surprising finding that time-staggered EGFR inhibition, but not simultaneous co-administration, can dramatically sensitize the apoptotic response of a subset of triple-negative cells to conventional DNA damaging agents. A systematic analysis of the order and timing of inhibitor/genotoxin presentation—using a combination of high-density time-dependent activity measurements of signaling networks, gene expression profiles, cell phenotypic responses, and mathematical modeling—revealed an approach for altering the intrinsic oncogenic state of the cell through dynamic re-wiring of oncogenic signaling pathways. This process converts these cells to a less tumorigenic state that is more susceptible to DNA damage-induced cell death, through re-activation of an extrinsic apoptotic pathway whose function is suppressed in the oncogene-addicted state. Three or 4 replicates of 3 different cell lines at time points 0minutes, 30minutes, 6 hours and 1 day after EGFR inhibition with erlotinib

2012-05-14 | E-GEOD-30516 | biostudies-arrayexpress

ATR inhibition rewires cellular signaling networks in response to pathologic replication stress

Project description:DNA replication stress is the major cause of genomic instability in human cells. The ataxia telangiectasia and Rad3-related kinase (ATR) plays an essential role in the cellular response to replication stress and inhibition of ATR has emerged as therapeutic strategy for the treatment of cancer. However, the ATR-dependent signaling in the cellular response to replication stress has not been systematically investigated. Here, we employ quantitative mass spectrometry-based proteomics to decipher the ATR-dependent phosphorylation events in response to pathological replication stress induced by hydroxyurea. Our data define the substrate spectrum of ATR and identify several novel putative ATR substrates. In addition, we demonstrate that ATR-inhibition fundamentally rewires cellular signaling networks leading to the prominent activation of different pathways including the ATM-driven double strand break repair.

2017-03-29 | MSV000080795 | MassIVE

Global transcriptome analysis of Rhizobium favelukesii LPU83 in response to acid stress.

Project description:Global transcriptome analysis of Rhizobium favelukesii LPU83 in response to acid stress.

| PRJNA594606 | ENA

Stress response in yeasts

Project description:Stress response in yeasts

| PRJNA108427 | ENA

Oxytocin Signaling Regulates the Homeostatic Response to Cold Stress in Ectothermic Vertebrate

Project description:Oxytocin Signaling Regulates the Homeostatic Response to Cold Stress in Ectothermic Vertebrate

| PRJNA667431 | ENA

Global assessment of integrated stress response in CF patients lung explants and organoids

Project description:Global assessment of integrated stress response in CF patients lung explants and organoids