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Selected Publication:

SHR Neuro Cancer Cardio Lipid

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 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG


Authors Med Uni Graz:
Al-Zoughbi Wael
Graier Wolfgang
Hoefler Gerald
Madl Tobias
Madreiter-Sokolowski Corina
Stryeck Sarah

Dimensions Citations:

Plum Analytics:
Number of Figures: 7
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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.

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