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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Project ID:PR001347
Project DOI:doi: 10.21228/M8M417
Project Title:GCN2 deletion influenced the energy metabolism in HSPCs.
Project Summary:Hematopoietic stem cells (HSCs) adapt their metabolism to maintenance and proliferation, but the mechanism remains incompletely understood. Here, we demonstrated that homeostatic HSCs had high amino acid (AA) catabolism to reduce the cellular AA levels, which activated the GCN2-eIF2α axis, a protein-synthesis-inhibitory checkpoint to inhibit protein synthesis for maintenance. Furthermore, upon proliferation conditions, HSCs increased mitochondrial oxidative phosphorylation (OXPHOS) for higher energy production but decreased AA catabolism to accumulate cellular AAs, which inactivated the GCN2-eIF2α axis to increase protein synthesis and coupled with proteotoxic stress. Importantly, GCN2 deletion impaired HSC function in repopulation and regeneration. Mechanistically, GCN2 maintained proteostasis and inhibited Src mediated AKT activation to repress mitochondrial OXPHOS in HSCs. Moreover, glycolytic metabolite, NAD+ precursor nicotinamide riboside (NR), accelerated AA catabolism to activate GCN2 and sustain long-term function of HSCs. Overall, our study uncovers the direct links between metabolic alterations and translation control in HSCs during homeostasis and proliferation.
Institute:Sun Yat-sen University
Last Name:Zhao
First Name:Meng
Address:Zhongshan 2nd Road