Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Glutaminolysis contribution to the carbon backbone of aspartate and glutamate in ccRCC

ABSTRACT: The objective of this experiment is to test the contribution of the carbons derived from glutamine to the generation of aspartate and glutamate in human epithelial renal cells HK2 and ccRCC cell lines 786-O and 786-M1A. To test this hypothesis, we incubated all cells with 13C5-glutamine in Plasmax media with or without a pharmacological inhibitor of glutaminase CB-839. This is Part 7 of a study and the experimental number is MS57.

ORGANISM(S): Human Homo Sapiens

TISSUE(S): Cultured Cells

DISEASE(S): Cancer

SUBMITTER: Ming Yang

PROVIDER: ST002222 | MetabolomicsWorkbench | Fri Jul 15 00:00:00 BST 2022

REPOSITORIES: MetabolomicsWorkbench

ACCESS DATA

Json Xml

Similar Datasets

Glutaminolysis contribution to the carbon backbone of aspartate through ATP Citrate Lyase (ACLY) in ccRCC

Project description:The objective of this experiment is to test the contribution of the carbons from glutamine to generation of aspartate via ATP citrate lyase (ACLY) in human epithelial renal cells HK2 and ccRCC cell lines 786-O and 786-M1A. To test this hypothesis, we incubated all cells with 13C5-glutamine in Plasmax media with or without a pharmacological inhibitor of ACLY. This is Part 8 of the study and the experimental number is MS58.

2022-07-15 | ST002221 | MetabolomicsWorkbench

Assessing the contribution of branched-chain amino acid (BCAA)-derived nitrogen to amino acid biosynthesis in renal cell lines HK2 and 786-O.

Project description:The objective of this experiment is to test the contribution of branched-chain amino acids (BCAA)-derived nitrogen to the generation of de novo amino acids in renal cells through transamination reactions. To test this hypothesis, we incubated human renal epithelial cell line HK2 and ccRCC cell lines 786-O, 786-M1A and 786-M2A with 15N-leucine and 15N-isoleucine in Plasmax media for 27h. Data were generated from 5 independent cultures. This is Part 2 of the study and the experimental number is MS48.

2022-07-15 | ST002227 | MetabolomicsWorkbench

Time sensitive contribution of the BCAA catabolism to the TCA cycle carbons in HK2, 786-O, OS-RC-2 and RFX-631

Project description:The objective of this experiment is to test the contribution of the branched chain amino acids catabolism to the carbons used in the TCA cycle. To test this hypothesis, we incubated human renal epithelial cells (HK2) and ccRCC cell lines (786-O, 786-M1A, OS-RC-2, OS-LM1, RFX-631) with 13C6-leucine and 13C6-isoleucine in Plasmax media for 10 mins, 1 hour and 3 hours. Data were generated from 5 independent cultures. This is Part 4 of the study and the experiment number is MS52.

2022-07-15 | ST002225 | MetabolomicsWorkbench

Intracellular metabolic profile of renal cells cultured in Plasmax

Project description:The objective of this experiment is to analyse the metabolic profiles of human renal epithelial cells HK2 and ccRCC cell lines 786-O, 786-M1A and 786-M2A in Plasmax media. The experiment was conducted on three different days using cells with different passage numbers. This is Part 5 of a study and the experimental number is MS55.

2022-07-15 | ST002224 | MetabolomicsWorkbench

Exometabolomics of HK2, 786-O cells cultured in Plasmax media

Project description:The objective of this study is to analyse the exometabolomics of human epithelial renal cell line HK2 and clear cell renal cell carcinoma (ccRCC) cell lines 786-O, 786-M1A, 786-M2A, OS-RC-2, OS-LM1 and RFX-631 that are cultured with the Plasmax media. This is part 3 of the study, and the experimental number is MS51.

2022-07-15 | ST002226 | MetabolomicsWorkbench

Catabolism of branched-chain amino acids (BCAAs) in renal cells HK2 and 786-O

Project description:The objective of this experiment is to compare the catabolism of branched-chain amino acids (BCAAs) in human renal epithelial cell line HK2 versus ccRCC cell lines 786-O, 786-M1A and 786-M2A using 13C6-labelled leucine and isoleucine stable isotope tracers. To this end, we incubated the above cell lines with 13C6-leucine and 13C6-isoleucine in Plasmax media for 27h. Data were generated from 5 independent cultures. This is Part I of the study and the experimental number is MS42.

2022-07-15 | ST002220 | MetabolomicsWorkbench

Differential effects of glutamine inhibition strategies on anti-tumor CD8 T cell function

Project description:Activated T cells undergo metabolic reprogramming to meet anabolic, differentiation, and functional demands. Glutamine supports many processes in activated T cells, and inhibition of glutamine metabolism alters T cell function in autoimmune disease and cancer. Multiple glutamine-targeting molecules are under investigation, yet the precise mechanisms of glutamine-dependent CD8 T cell differentiation remain unclear. We show that distinct strategies of glutamine inhibition by glutaminase-specific inhibition with small molecule CB-839, pan-glutamine inhibition with 6-diazo-5-oxo-L-norleucine (DON), or by glutamine deprivation (No Q) produce distinct metabolic differentiation trajectories in CD8 T cells. T cell activation with CB-839 treatment had a milder effect than DON or No Q treatment. A key difference was that CB-839-treated cells compensated with increased glycolytic metabolism, while DON and No Q-treated cells increased oxidative metabolism. However, all glutamine treatment strategies elevated CD8 T cell dependence on glucose metabolism, and No Q treatment caused adaptation toward reduced glutamine dependence. DON treatment reduced histone modifications and numbers of memory-like cells in adoptive transfer studies, but those T cells that persisted could expand normally upon secondary antigen encounter. In contrast, No Q-treated cells persisted well yet demonstrated decreased secondary expansion. Consistent with impaired function, CD8 T cells activated in the presence of DON had reduced ability to control tumor growth and reduced tumor infiltration in adoptive cell therapy. Overall, each approach to inhibit glutamine metabolism confers distinct effects on CD8 T cells and highlights that targeting the same pathway in different ways can elicit opposing metabolic and functional outcomes.

2023-05-12 | GSE232241 | GEO

Reversible and Dynamic m1A Methylation in the Human Transcriptome

Project description:N1-methyladenosine (m1A) is an abundant post-transcriptional RNA modification, yet little is known about its prevalence, topology and dynamics in mRNA. Here, we show that m1A is abundant in human mRNA, with an m1A/A ratio of ~0.02%. We develop m1A-ID-Seq, based on m1A immunoprecipitation and the inherent property of m1A to stall reverse transcription, for the transcriptome-wide m1A analysis. m1A-ID-Seq identifies 901 m1A peaks (from 583 genes) in mRNA and ncRNA, and reveals a prominent feature of enrichment in the 5â-untranslated region of mRNA transcripts, distinct from that of N6-methyladenosine, the most abundant internal mammalian mRNA modification. m1A in mRNA is also reversible by ALKBH3, a known DNA/RNA demethylase. Lastly, m1A responds dynamically to stimuli and hundreds of stress-induced m1A sites are identified. Collectively, our approaches allow comprehensive analysis of m1A methylation and provide an important tool for functional studies of potential epigenetic regulation via the reversible and dynamic m1A methylation. Identification of m1A sites in human embryonic kidney cells. Comparisons of m1A profiles of wild type HEK293T with ALKBH3 knock out cell line reveals the ALKBH3 specific sites. Stress inducible m1A sites are also identified by comparing the profiles of untreated cells with stress treated cells.

2016-02-05 | E-GEOD-73941 | biostudies-arrayexpress

Analyzing the impact of Mycobacterium tuberculosis infection on primary human macrophages

Project description:The success of Mycobacterium tuberculosis (Mtb) as pathogen is tightly linked to its ability to recalibrate host metabolic processes in infected host macrophages. Correspondingly, analysis of RNA-sequencing datasets showed altered gene expression of key metabolic enzymes involved in NAD+, creatine, glucose and glutamine metabolism (e.g NAMPT, IDO1, SLC6A8, CKB, HK2) in Mtb-infected M2 macrophages.

2020-04-16 | GSE148731 | GEO