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Transcriptomic analysis of GLUD1-knockdown 786-0 cells under amino acid deprivation

ABSTRACT: Transcriptomic analysis of GLUD1-knockdown 786-0 cells under amino acid deprivation

PROVIDER: PRJNA704839 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13783109_1.fastq.gz	Fastqsanger.gz
	SRR13783109_2.fastq.gz	Fastqsanger.gz
	SRR13783110_1.fastq.gz	Fastqsanger.gz
	SRR13783110_2.fastq.gz	Fastqsanger.gz
	SRR13783111_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of GLUD1-knockdown 786-0 cells under amino acid deprivation

Project description:shGLUD1 and shNT 786-0 cells were pretreated by amino acid starvation for 12 hours, then total mRNA were extracted for sequencing.

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Project description:We present transcriptome profiling of 786-0 renal cell carcinoma cell lines both with and without Everolimus, an mTOR inhibitorhbn

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DA Methylation patterns in decitabine treated 786-0 cells

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786-O and 786-VHL in EMCV study

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786-O and 786-VHL in EMCV study

Project description:786-0 is a cell line derived from a clear cell renal carcinoma. Previous studies have shown that the 786-O cell line harbors an inactivating mutation in the von-Hippel Lindau (VHL) gene. Mutations in the VHL gene occur in the majority of sporadic clear cell renal cell. To determine how inactivation of the VHL affects cellular functions, we created a derivative of 786-0, which we call 786-VHL in which a functional allele of VHL has been introduced back into the 786-O cell line. The renal cell carcinoma cell line 786-0, which harbors a mutated allele of VHL, was compared to a cell line derived from 786-0, termed 786-VHL, that contains a functional allele of VHL. Genes whose expression characteristics were dependent on functional VHL were identified.

2010-06-23 | E-GEOD-22256 | 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 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.

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RNA-seq of a VHL-/- human renal cancer cell line 786-0 transfected with 3 vectors

Project description:The human renal cancer cell line 786-0 was transfected with 3 vectors allowing the doxycycline-inducible expression of 1) the full length wild type sequence of VHL: 786-0 VHL WT, VHL+/+, 2) the R167Q mutant : 786-0 R167Q, VHL mutated, 3) the empty vector : 786-0 EV, VHL-/-. The aim of the study was to examine whether the VHL-R167Q mutation, which is associated with a high risk of developping clear cell renal carcinomas, could impact the plasticity of renal carcinoma cells.

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Gene expression profiling of 786-O cells with ZHX2 and p65 knockdown

Project description:We are examining the regulatory pathway of ZHX2 and p65 in clear cell renal cell carcinoma cell line 786-O

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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.

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