Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dynlrb1 is Essential for Dynein Mediated Transport and Neuronal Survival

ABSTRACT: Dynlrb1 is Essential for Dynein Mediated Transport and Neuronal Survival

PROVIDER: PRJNA543760 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Dynlrb1 is Essential for Dynein Mediated Transport and Neuronal Survival

Project description:We identified Dynlrb1 as an essential gene for sensory neuron survival and performed RNA sequencing to identify the molecular mechanism mediating the role of Dynlrb1 in sensory neuron survival.

2020-03-04 | GSE131455 | GEO

DYNLRB1 is essential for dynein mediated transport and neuronal survival.

Project description: Not available

| S-EPMC7273200 | biostudies-literature

Neuroblastoma-associated mutations in Drosophila Alk peturb neuronal differentiation and promote neuronal survival.

Project description:Neuroblastoma-associated mutations in Drosophila Alk peturb neuronal differentiation and promote neuronal survival.

| PRJNA817171 | ENA

NAMPT-mediated NAD+ salvage is essential for mitochondrial function and swelling, muscle fiber integrity and premature survival

Project description:NAMPT-mediated NAD+ salvage is essential for mitochondrial function and swelling, muscle fiber integrity and premature survival

| PRJNA614906 | ENA

Neuronal mitochondria transport Pink1 mRNA via Synaptojanin 2 to support local mitophagy

Project description:Neuronal mitochondria transport Pink1 mRNA via Synaptojanin 2 to support local mitophagy

| PRJNA796269 | ENA

A cell fitness selection model for neuronal survival during development

Project description:A cell fitness selection model for neuronal survival during development

| PRJNA557677 | ENA

The General Transcription Factor TAF7 is Essential for Embryonic Development but Not Essential for the Survival or Differentiation of Mature T Cells

Project description:This SuperSeries is composed of the following subset Series: GSE34793: The General Transcription Factor TAF7 is Essential for Embryonic Development but Not Essential for the Survival or Differentiation of Mature T Cells (MEF data) GSE34795: The General Transcription Factor TAF7 is Essential for Embryonic Development but Not Essential for the Survival or Differentiation of Mature T Cells (T cell data) Refer to individual Series

2012-03-31 | E-GEOD-34796 | biostudies-arrayexpress

Negative feedback control of neuronal activity by microglia

Project description:Microglia, the brain resident macrophages, play a key role in the regulation of brain function by removing dying neurons, pruning non-functional synapses, and producing ligands that support neuronal survival. We have identified a new function of microglia as critical modulators of neuronal activity and associated behavioral responses in mice. We show that microglia respond to neuronal activation and that ablation of microglia amplifies and synchronizes the activity of neurons, leading to seizures. The suppressive impact of microglia on neuronal activation occurs in a highly localized fashion and depends on the ability of microglia to sense and catabolize extracellular ATP. ATP, which can be released upon neuronal activation by neurons and astrocytes, triggers the recruitment of microglia protrusions and is converted by the microglial ATP-hydrolyzing enzyme CD39 and CD73 into AMP and adenosine, a potent suppressor of neuronal activity. We show that the microglial sensing of ATP, the ensuing production of adenosine, and the adenosine-mediated control of neuronal response via the A1R are essential for the microglia-mediated regulation of neuronal activity and animal behavior. Our findings suggest that this microglia-driven negative feedback mechanism operates in a fashion similar to inhibitory neurons and plays an essential role in protecting the brain from excessive activation in health and diseases.

2020-08-18 | GSE149897 | GEO

Evidence for a rheostat that determines neuronal survival after traumatic brain injury

Project description:To investigate the determinants of neuronal survival after traumatic brain injury, we compared the transcriptional profiles of dying (Fluoro-Jade-positive) and immediately adjacent surviving (Fluoro-Jade-negative) neurons from the CA3 subfield of the rat hippocampus 24 hours after experimental TBI. We found that hippocampal neurons that survive TBI invariably express high levels of genes that have cellular functions involved in survival, regeneration, development, proliferation, neuronal plasticity such as cAMP response element binding protein (CREB), brain-derived-neurotrophic factor (BDNF) and mitogen-activated protein kinase 1 (MAPK1). Dying neurons express high levels of genes involved in aberrant cell cycle progression, immune response, inflammation, oxidative stress and apoptosis such as Interleukin-1β (IL-1β), caspase 3 and B-cell linker (BLNK). We conclude that shifting the balance between the global levels of these proteins with pharmacotherapeutic drugs that induce expression of cell survival associated genes, is expected to alter the cellular rheostat that determines cell survival or cell death. Replicate pooled samples (approximately 600 laser capture microdissected hippocampal neurons per sample of dying neurons (labeled with Fluoro-Jade, a fluorescent stain for degenerating CNS neurons) and surviving neurons (Fluoro-Jade-negative) were hybridized in duplicate to rat Agilent whole genome arrays.

2010-12-20 | E-GEOD-16735 | biostudies-arrayexpress

HtrA1-dependent proteolysis of TGF-M-NM-2 controls both neuronal maturation and developmental survival

Project description:Transforming growth factor-M-NM-2 (TGF-M-NM-2) signalling controls a number of cerebral functions and dysfunctions including synaptogenesis, amyloid-M-NM-2 accumulation, apoptosis and excitotoxicity. Using cultured cortical neurons prepared from either wild type or transgenic mice over-expressing a TGF-M-NM-2 responsive luciferase reporter gene (SBE-Luc), we demonstrated a progressive loss of TGF-M-NM-2 signalling during neuronal maturation and survival. Moreover, we showed that neurons exhibit increasing amounts of the serine protease HtrA1 (high temperature responsive antigen 1) and corresponding cleavage products during both in vitro neuronal maturation and brain development. In parallel of its ability to promote degradation of TGF-M-NM-21, we demonstrated that blockage of the proteolytic activity of HtrA1 leads to a restoration of TGF-M-NM-2 signalling, subsequent overexpression of the serpin type -1 plasminogen activator inhibitor (PAI-1) and neuronal death. Altogether, we propose that the balance between HtrA1 and TGF-M-NM-2 could be one of the critical events controlling both neuronal maturation and developmental survival. Keywords: HtrA1 / neuronal survival / PAI-1 / TGF-M-NM-2 signalling / tPA Total RNA were extracted from 3 cultures of 2 DIV Human neurons. For each stage, equal amounts of each RNA were pooled and 5M-BM-5g were reverse-transcribed, labelled and hybridized on pangenomic microarrays. Each pool was hybridized in duplicate dye-swap independent experiments.

2008-04-15 | E-GEOD-11162 | biostudies-arrayexpress

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