Transformation by the (R)-enantiomer of 2-hydroxyglutarate linked to EGLN activation

Peppi Koivunen, Sungwoo Lee, Christopher G. Duncan, Giselle Lopez, Gang Lu, Shakti Ramkissoon, Julie A. Losman, Päivi Joensuu, Ulrich Bergmann, Stefan Gross, Jeremy Travins, Samuel Weiss, Ryan Looper, Keith L. Ligon, Roel G. W. Verhaak, Hai Yan and William G. Kaelin ()
Additional contact information
Peppi Koivunen: Biocenter Oulu, Oulu Center for Cell-Matrix Research, University of Oulu, FIN-90014 Oulu, Finland
Sungwoo Lee: Dana-Farber Cancer Institute and Brigham and Women’s Hospital, Boston, Massachusetts 02215, USA
Christopher G. Duncan: The Preston Robert Tisch Brain Tumor Center at Duke, Duke University Medical Center
Giselle Lopez: The Preston Robert Tisch Brain Tumor Center at Duke, Duke University Medical Center
Gang Lu: Dana-Farber Cancer Institute and Brigham and Women’s Hospital, Boston, Massachusetts 02215, USA
Shakti Ramkissoon: Dana-Farber Cancer Institute and Brigham and Women’s Hospital, Boston, Massachusetts 02215, USA
Julie A. Losman: Dana-Farber Cancer Institute and Brigham and Women’s Hospital, Boston, Massachusetts 02215, USA
Päivi Joensuu: University of Oulu, FIN-90014 Oulu, Finland
Ulrich Bergmann: Biocenter Oulu, Mass Spectrometry Core Facility, University of Oulu, FIN-90014 Oulu, Finland
Stefan Gross: Agios Pharmaceuticals
Jeremy Travins: Agios Pharmaceuticals
Samuel Weiss: Hotchkiss Brain Institute, University of Calgary Faculty of Medicine, Calgary, Alberta T2N 4N1, Canada
Ryan Looper: University of Utah
Keith L. Ligon: Dana-Farber Cancer Institute and Brigham and Women’s Hospital, Boston, Massachusetts 02215, USA
Roel G. W. Verhaak: University of Texas MD Anderson Cancer Center
Hai Yan: The Preston Robert Tisch Brain Tumor Center at Duke, Duke University Medical Center
William G. Kaelin: Dana-Farber Cancer Institute and Brigham and Women’s Hospital, Boston, Massachusetts 02215, USA

Nature, 2012, vol. 483, issue 7390, 484-488

Abstract: The (R)-enantiomer of 2-hydroxyglutarate, which is produced when IDH is mutated in human tumours, is shown to stimulate the activity of the EGLN prolyl 4-hydroxylases, leading to diminished levels of HIF and enhanced human astrocyte proliferation.

Date: 2012
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/nature10898 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:483:y:2012:i:7390:d:10.1038_nature10898

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/nature10898

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().