Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Navigation/Suche
- Forscher*innen
- Institutionen
- Projekte
- Publikationen
- Partner
- Geldgeber
- Ausstattung
- Knowhow
- Forschungsfelder
"Köpfe" der aktuellen Meldungen:
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Alkan, HF; Walter, KE; Luengo, A; Madreiter-Sokolowski, CT; Stryeck, S; Lau, AN; Al-Zoughbi, W; Lewis, CA; Thomas, CJ; Hoefler, G; Graier, WF; Madl, T; Vander Heiden, MG; Bogner-Strauss, JG.
Cytosolic Aspartate Availability Determines Cell Survival When Glutamine Is Limiting.
Cell Metab. 2018; 28(5):706-720
Doi: 10.1016/j.cmet.2018.07.021
[OPEN ACCESS]
Web of Science
PubMed
FullText
FullText_MUG
- Co-Autor*innen der Med Uni Graz
- Al-Zoughbi Wael
- Graier Wolfgang
- Höfler Gerald
- Madl Tobias
- Madreiter-Sokolowski Corina
- Stryeck Sarah
- Altmetrics:
- Dimensions Citations:
- Plum Analytics:
- Scite (citation analytics):
- Abstract:
- Mitochondrial function is important for aspartate biosynthesis in proliferating cells. Here, we show that mitochondrial aspartate export via the aspartate-glutamate carrier 1 (AGC1) supports cell proliferation and cellular redox homeostasis. Insufficient cytosolic aspartate delivery leads to cell death when TCA cycle carbon is reduced following glutamine withdrawal and/or glutaminase inhibition. Moreover, loss of AGC1 reduces allograft tumor growth that is further compromised by treatment with the glutaminase inhibitor CB-839. Together, these findings argue that mitochondrial aspartate export sustains cell survival in low-glutamine environments and AGC1 inhibition can synergize with glutaminase inhibition to limit tumor growth. Copyright © 2018. Published by Elsevier Inc.