Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

GeneChip expression profiling of Glud1 (glutamate dehydrogenase 1) transgenic mice across age

ABSTRACT: Glud1 (Glutamate dehydrogenase 1) transgenic mice release more excitatory neurotransmitter glutamate to synaptic cleft throughout lifespan. Here we compared transcriptomic profiles of these animals to their wild-type counterparts across 5 ages. The hippocampus was used for the analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE48911 | GEO | 2014/07/31

SECONDARY ACCESSION(S): PRJNA212284

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

GeneChip expression profiling of Glud1 (glutamate dehydrogenase 1) transgenic mice across age

Project description:Glud1 (Glutamate dehydrogenase 1) transgenic mice release more excitatory neurotransmitter glutamate to synaptic cleft throughout lifespan. Here we compared transcriptomic profiles of these animals to their wild-type counterparts across 5 ages. The hippocampus was used for the analysis. Longitudinal studies of Glud1 transgenic and wide-type mice across 5 age points: 10 days post birth, 4.5 mo, 9 mo, 14.5 mo, and 20 mo.

2014-07-31 | E-GEOD-48911 | biostudies-arrayexpress

GeneChip expression profiling of Glud1 (glutamate dehydrogenase 1) transgenic mice

Project description:Glud1 (glutamate dehydrogenase 1) transgenic mice release more excitatory neurotransmitter glutamate to synaptic cleft throughout lifespan and show signs of accelerated aging. Here we compared transcriptomic profiles of these animals to their wild-type counterparts. The hippocampus was used for the analysis. Keywords: transgenic analysis Three Glud1 transgenic mice vs. three age-matched wide-type mice. Age: 9-month-old. Tissue: hippocampus.

2010-07-12 | E-GEOD-11419 | biostudies-arrayexpress

GeneChip expression profiling of Glud1 (glutamate dehydrogenase 1) transgenic mice

2010-07-12 | GSE11419 | GEO

GLUD1 determines murine muscle stem cell fate by controlling mitochondrial glutamate levels

Project description:Muscle stem cells (MuSCs) enable muscle growth and regeneration after exercise or injury, but how metabolism controls their regenerative potential is poorly understood. We describe that primary metabolic changes can determine murine MuSC fate decisions. We found that glutamine anaplerosis into the TCA cycle decreases during MuSC differentiation and coincides with decreased expression of the mitochondrial glutamate deaminase GLUD1. Deletion of Glud1 in proliferating MuSCs resulted in precocious differentiation and fusion combined with loss of self-renewal in vitro and in vivo. Mechanistically, deleting Glud1 caused mitochondrial glutamate accumulation and inhibited the malate-aspartate shuttle (MAS). The resulting defect in transporting NADH reducing equivalents into the mitochondria induced compartment-specific NAD+/NADH ratio shifts. MAS activity restoration or directly altering NAD+/NADH ratios normalised myogenesis. In conclusion, GLUD1 prevents deleterious mitochondrial glutamate accumulation and inactivation of the MAS in proliferating MuSCs. It thereby acts as a compartment specific metabolic brake on MuSC differentiation.

2024-07-02 | GSE243640 | GEO

Redirected nuclear glutamate dehydrogenase supplies Tet3 with a-ketoglutarate in neurons

Project description:Tet3 is an Fe2+-dependent enzyme that oxidizes genomic 5-methylcytosine to 5-hydroxymethylcytosine with the help of alpha-ketoglutarate and oxygen. It is the most abundant Tet enzyme in differentiated tissues including brain. Adult brain contains the highest 5-hydroxymethylcytosine levels. How alpha-ketoglutarate is made available for the oxidation of mC in brain cells and how the Tet activity is linked to neural activity are unsolved questions. Our experiments with full mouse brains show that Tet3 interacts in the nucleus directly with selected enzymes of the mitochondrial citric acid cycle. This leads to the formation of isocitrate. Tet3 also interacts with aspartate aminotransferase, which produces oxaloacetate. Although oxaloacetate and isocitrate are biosynthetic alpha-ketoglutarate precursors, they function as inhibitors of Tet3 and are needed to protect the reactive Fe2+ center from degrading DNA. The supply of Tet3 with alpha-ketoglutarate is established by a direct interaction of Tet3 with glutamate dehydrogenase (Glud1), which converts the neurotransmitter glutamate directly into alpha-ketoglutarate. This links Tet3 function to neural activity.

2021-05-10 | PXD004518 | Pride

Glutamate-induced transcriptional changes in embryonic mouse cortical neurons [GRO-seq]

Project description:Glutamate is a major excitatory neurotransmitter in the nervous system. Increased and persistent release of glutamate is toxic to neurons and this excitotoxicity is a hallmark of several neurodegenerative diseases. Here, we use GRO-seq to screen for the acute transcriptional changes induced by glutamate exposure on embryonic mouse cortical neurons to reveal downstream molecules which could participate in glutamate-induced toxicity. We show that several miRNA genes, such as miR-21, have altered expression upon glutamate exposure.

2023-01-03 | GSE215210 | GEO

ABCC5 functions as a transporter of glutamate conjugates and analogs

Project description:The ubiquitous efflux transporter ATP-binding cassette sub-family C member 5 (ABCC5) is present at high levels in the blood-brain barrier, neurons and glia, but its in vivo substrates and function are not known. Untargeted metabolomic screens revealed that Abcc5-/- mice accumulate endogenous glutamate conjugates and analogs in several tissues, but brain in particular. The abundant neurotransmitter N-acetylaspartylglutamate (NAAG), for example, was over 2-fold higher in Abcc5-/- brain. In line with ABCC5-mediated transport, the metabolites that accumulated in Abcc5-/- tissues were depleted in cultured cells that overexpressed human ABCC5. Using membrane vesicles, we show that ABCC5 not only transports the metabolites detected in our screen, but also a wide range of peptides containing a C-terminal glutamate. Glutamate conjugates are of physiological relevance because they can affect the function of glutamate, the principal excitatory neurotransmitter in the brain. We found that ABCC5 also transports exogenous glutamate analogs, like the classic excitotoxic neurotoxins kainic acid, domoic acid and N-methyl-D-aspartate (NMDA) and the therapeutic glutamate analog ZJ43. Taken together, we have identified ABCC5 as a general glutamate conjugate and analog transporter that affects the disposition of endogenous metabolites, toxins and drugs.

2015-10-01 | GSE68628 | GEO

Identification of glutamate receptor delta-1 interactome at synapses.

Project description:In this project, we have investigated the interactome of the glutamate receptor delta-1 (GluD1) in developing synapses in mice. GluD1 is a member of the delta subfamily of ionotropic glutamate receptors widely expressed in the brain. It behaves as a postsynaptic organizer by engaging in trans-synaptic interaction and by mediating postsynaptic signaling.

2019-11-06 | PXD010373 | Pride

Global gene profiling of glutamate-induced neuronal death

2013-12-31 | GSE19936 | GEO

Global gene profiling of glutamate-induced neuronal death

Project description:Glutamate, a major neurotransmitter in the mammalian nervous sytem, has been involved in the mediation of excitotoxicity commonly observed in the pathogenesis of stroke. Current study focused on gaining an insight into the molecular mechanisms of glutamate-induced neuronal death A total of 15 RNA samples were analyzed. There is one treatment conditions of 250uM glutamate. 3 replicates were collected for each of the selected time-points (5h, 15h and 24h) in addition to 6 replicates of shared vehicle control.

2013-12-31 | E-GEOD-19936 | 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