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Mus musculus

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

OTHER RELATED OMICS DATASETS IN: E-GEOD-48911

PROVIDER: PRJNA212284 | ENA |

REPOSITORIES: ENA

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Mus musculus

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

| PRJNA106435 | ENA

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

E-GEOD-48911

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

2015-07-21 | E-GEOD-48911 | ExpressionAtlas

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

2010-07-12 | GSE11419 | GEO

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

2014-07-31 | GSE48911 | GEO

Mice carrying a human GLUD2 gene recapitulate aspects of human transcriptome and metabolome development

Project description:Whereas all mammals have one glutamate dehydrogenase gene (GLUD1), humans and apes carry an additional gene (GLUD2), which encodes an enzyme with distinct biochemical properties. We inserted human genomic region containing the GLUD2 gene into mice and analyzed the resulting changes in the transcriptome and metabolome during postnatal brain development. Effects were most pronounced early postnatally and affected predominantly genes involved in neuronal development. Remarkably, the effects in the transgenic mice partially parallel the transcriptome and metabolome differences seen between humans and macaques analyzed. Notably, the introduction of GLUD2 did not affect glutamate levels in mice, consistent with observations in the primates. Instead, the metabolic effects of GLUD2 center on the tricarboxylic acid cycle, suggesting that GLUD2 affects carbon flux during early brain development, possibly stimulating lipid biosynthesis.

2016-04-27 | GSE80122 | 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

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

Non-canonical glutamine transamination sustains efferocytosis by coupling redox buffering to oxidative phosphorylation

Project description:Macrophages rely on tightly integrated metabolic rewiring to clear dying neighboring cells by efferocytosis during homeostasis and disease. Here, we reveal that glutaminase (GLS) 1-mediated glutaminolysis is critical to promote apoptotic cell clearance by macrophages during homeostasis in mice. In addition, impaired macrophage glutaminolysis exacerbates atherosclerosis, a condition during which efficient apoptotic cell debris clearance is critical to limit disease progression. Gls1 expression strongly correlates with atherosclerotic plaque necrosis in patients with cardiovascular diseases. High-throughput transcriptional and metabolic profiling revealed that macrophage efferocytic capacity relies on a non-canonical transaminase pathway, independent from the traditional requirement of glutamate dehydrogenase (GLUD1) to fuel ɑ-ketogulatrate-dependent immunometabolism. This pathway is necessary to meet the unique requirements of efferocytosis for cellular detoxification and high energy cytoskeletal rearrangements. Thus, we uncovered a novel role for non-canonical glutamine metabolism for efficient clearance of dying cells and maintenance of tissue homeostasis during health and disease in mouse and humans

2021-12-31 | GSE183176 | GEO

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