Summary of Study ST002123

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, where it has been assigned Project ID PR001347. The data can be accessed directly via it's Project DOI: 10.21228/M8M417 This work is supported by NIH grant, U2C- DK119886.


This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST002123
Study TitleGCN2 regulates mitochondrial OXPHOS in HSPCs under proliferation conditions.
Study SummaryOur results revealed that among all 273 metabolites detected, the levels of metabolites involved in glucose-related glycolysis and gluconeogenesis were elevated in GCN2 deleted HSPCs. Moreover, GCN2 deletion specifically increased mitochondrial OXPHOS and suppressed anaerobic glycolysis in HSPCs.
Sun Yat-sen University
Last NameZhao
First NameMeng
AddressZhongshan 2nd Road
Submit Date2022-04-05
Raw Data AvailableYes
Raw Data File Type(s)wiff
Analysis Type DetailLC-MS
Release Date2022-11-01
Release Version1
Meng Zhao Meng Zhao application/zip

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Treatment ID:TR002220
Treatment Summary:Wild-type and GCN2 knockout mice were intraperitoneally injected with 10 mg/kg 5FU (F6627-5G, Sigma-Aldrich) for 14 days. HSPCs were stained and sorted from treated mice.