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.
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.
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
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.
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.
Project description:Here we identified a role for the lncRNA MYLK-AS1 promoting acquired TKI resistance of lung cancer in vitro and in vivo. MYLK-AS1 bound and directly drove phase separation of interleukin enhancer binding factor 3 (ILF3), thus interacting with the 3’UTR of glutamate dehydrogenase 1 (GLUD1) to post-transcriptionally promote its mRNA stability, thus enhancing mitochondrial glutamine catabolism, promoting TKI resistance. The MYLK-AS1/ILF3/GLUD1 may be a target for overcoming TKI resistance in lung cancer.
Project description:Transcription profiling of transgenic mice overexpressing human alpha-synuclein under the PDGF beta promoter to wildtype littermates at 3 months and 9 months of age.