Correcting glucose-6-phosphate dehydrogenase deficiency with a small-molecule activator
Abstract
Here, glucose-6-phosphate dehydrogenase (G6PD) deficiency, one of the most common human genetic enzymopathies, is caused by over 160 different point mutations and contributes to the severity of many acute and chronic diseases associated with oxidative stress, including hemolytic anemia and bilirubin-induced neurological damage particularly in newborns. As no medications are available to treat G6PD deficiency, here we seek to identify a small molecule that corrects it. Crystallographic study and mutagenesis analysis identify the structural and functional defect of one common mutant (Canton, R459L). Using high-throughput screening, we subsequently identify AG1, a small molecule that increases the activity of the wild-type, the Canton mutant and several other common G6PD mutants. AG1 reduces oxidative stress in cells and zebrafish. Furthermore, AG1 decreases chloroquine- or diamide-induced oxidative stress in human erythrocytes. Our study suggests that a pharmacological agent, of which AG1 may be a lead, will likely alleviate the challenges associated with G6PD deficiency.
- Authors:
-
[1];
[1];
[3];
[1];
[1]
- Stanford Univ., Stanford, CA (United States)
- Stanford Univ., Stanford, CA (United States); Chapman Univ., Irvine, CA (United States); SLAC National Accelerator Lab., Menlo Park, CA (United States)
- Stanford Univ., Stanford, CA (United States); The Ohio State Univ., Columbus, OH (United States); Univ. of Wyoming School of Pharmacy, Laramie, WY (United States)
- Publication Date:
- Research Org.:
- SLAC National Accelerator Laboratory (SLAC), Menlo Park, CA (United States)
- Sponsoring Org.:
- USDOE
- OSTI Identifier:
- 1490641
- Grant/Contract Number:
- AC02-76SF00515; HD084422
- Resource Type:
- Accepted Manuscript
- Journal Name:
- Nature Communications
- Additional Journal Information:
- Journal Volume: 9; Journal Issue: 1; Journal ID: ISSN 2041-1723
- Publisher:
- Nature Publishing Group
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 59 BASIC BIOLOGICAL SCIENCES; 60 APPLIED LIFE SCIENCES
Citation Formats
Hwang, Sunhee, Mruk, Karen, Rahighi, Simin, Raub, Andrew G., Chen, Che -Hong, Dorn, Lisa E., Horikoshi, Naoki, Wakatsuki, Soichi, Chen, James K., and Mochly-Rosen, Daria. Correcting glucose-6-phosphate dehydrogenase deficiency with a small-molecule activator. United States: N. p., 2018.
Web. doi:10.1038/s41467-018-06447-z.
Hwang, Sunhee, Mruk, Karen, Rahighi, Simin, Raub, Andrew G., Chen, Che -Hong, Dorn, Lisa E., Horikoshi, Naoki, Wakatsuki, Soichi, Chen, James K., & Mochly-Rosen, Daria. Correcting glucose-6-phosphate dehydrogenase deficiency with a small-molecule activator. United States. https://doi.org/10.1038/s41467-018-06447-z
Hwang, Sunhee, Mruk, Karen, Rahighi, Simin, Raub, Andrew G., Chen, Che -Hong, Dorn, Lisa E., Horikoshi, Naoki, Wakatsuki, Soichi, Chen, James K., and Mochly-Rosen, Daria. Tue .
"Correcting glucose-6-phosphate dehydrogenase deficiency with a small-molecule activator". United States. https://doi.org/10.1038/s41467-018-06447-z. https://www.osti.gov/servlets/purl/1490641.
@article{osti_1490641,
title = {Correcting glucose-6-phosphate dehydrogenase deficiency with a small-molecule activator},
author = {Hwang, Sunhee and Mruk, Karen and Rahighi, Simin and Raub, Andrew G. and Chen, Che -Hong and Dorn, Lisa E. and Horikoshi, Naoki and Wakatsuki, Soichi and Chen, James K. and Mochly-Rosen, Daria},
abstractNote = {Here, glucose-6-phosphate dehydrogenase (G6PD) deficiency, one of the most common human genetic enzymopathies, is caused by over 160 different point mutations and contributes to the severity of many acute and chronic diseases associated with oxidative stress, including hemolytic anemia and bilirubin-induced neurological damage particularly in newborns. As no medications are available to treat G6PD deficiency, here we seek to identify a small molecule that corrects it. Crystallographic study and mutagenesis analysis identify the structural and functional defect of one common mutant (Canton, R459L). Using high-throughput screening, we subsequently identify AG1, a small molecule that increases the activity of the wild-type, the Canton mutant and several other common G6PD mutants. AG1 reduces oxidative stress in cells and zebrafish. Furthermore, AG1 decreases chloroquine- or diamide-induced oxidative stress in human erythrocytes. Our study suggests that a pharmacological agent, of which AG1 may be a lead, will likely alleviate the challenges associated with G6PD deficiency.},
doi = {10.1038/s41467-018-06447-z},
journal = {Nature Communications},
number = 1,
volume = 9,
place = {United States},
year = {Tue Oct 02 00:00:00 EDT 2018},
month = {Tue Oct 02 00:00:00 EDT 2018}
}
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Works referencing / citing this record:
Small‐Molecule Activators of Glucose‐6‐phosphate Dehydrogenase (G6PD) Bridging the Dimer Interface
journal, June 2019
- Raub, Andrew G.; Hwang, Sunhee; Horikoshi, Naoki
- ChemMedChem, Vol. 14, Issue 14
Neuroprotection by glucose‐6‐phosphate dehydrogenase and the pentose phosphate pathway
journal, April 2019
- Tang, Bor Luen
- Journal of Cellular Biochemistry, Vol. 120, Issue 9
Discovery of Small-Molecule Activators for Glucose-6-Phosphate Dehydrogenase (G6PD) Using Machine Learning Approaches
journal, February 2020
- Saddala, Madhu Sudhana; Lennikov, Anton; Huang, Hu
- International Journal of Molecular Sciences, Vol. 21, Issue 4
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journal, February 2020
- Saddala, Madhu Sudhana; Lennikov, Anton; Huang, Hu
- International Journal of Molecular Sciences, Vol. 21, Issue 4