Glutaminase 2, a novel p53 target gene regulating energy metabolism and antioxidant function

By Wenwei Hu, Cen Zhang, R. Wu, Yvonne Y Sun, Arnold J. Levine, Zhaohui Feng. Proceedings of the National Academy of Sciences of the United States of America, 2010

841 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/2561a1293baf15672e2990761b5d4819a4d2721a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. C. V. Dang
2. Guido Kroemer
3. M. V. Vander Heiden
4. David M. Sabatini
5. L. Galluzzi
6. J. Cantor
7. D. Y. Gui
8. Alba Luengo

In Molecular Biology

1. C. V. Dang
2. Guido Kroemer
3. L. Galluzzi
4. Douglas R. Green
5. M. V. Vander Heiden
6. J. Cantor
7. David M. Sabatini
8. W. Gu

In Oncology

1. Guido Kroemer
2. L. Galluzzi
3. W. Gu
4. Yingming Zhao
5. N. Kon
6. Douglas R. Green
7. C. V. Dang
8. David M. Sabatini

Citations in the corpus

• The interaction between ferroptosis and lipid metabolism in cancer (2020, background): “On the one hand, P53 can promote the accumulation of lipid hydroperoxides to enhance ferroptosis by increasing the expression levels of 15-LOX by promoting the expression of spermidine/ spermine N1-acetyltransferase1 (STA1), or increasing the expression of GLS2, and activating the function of 12-LOX”
• Targeting Metabolism for Cancer Therapy (2017, background): “There is also data that GLS2 activity can be tumor suppressive (Hu et al., 2010), underscoring the importance of defining the patient population likely to benefit from glutaminase inhibition.”
• The transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation (2011, background): “Although recent studies indicate that the tumor suppressor p53 is required for the induction of GLS2 in a human tumor cell line (Hu et al., 2010; Suzuki et al., 2010),”
• Targeting mitochondrial glutaminase activity inhibits oncogenic transformation (2010, neutral): “Recently, it has been shown that the expression of a distinct form of glutaminase, referred to as the liver-type enzyme or GLS2, was substantially decreased in liver cancer cells and that its overexpression reduced colony formation (Hu et al., 2010; Suzuki et al., 2010).”
• Targeting cancer metabolism: a therapeutic window opens (2011, background): “, whereas GLS2 is regulated by the tumour suppressor p53 and influences the cellular redox state”
• Cancer Cell Metabolism: One Hallmark, Many Faces (2012, background): “Whereas Myc specifically potentiates elevated expression of GLS1 and promotes the downstream utilization of glutamine carbon in anaplerosis (55, 56), p53 specifically activates GLS2 to support cellular defense against oxidative stress (130).”
• Tumor suppression in the absence of p53-mediated cell cycle arrest, apoptosis, and senescence (2012, positive): “p53 also modulates production of glutamine, an alternative to glucose as a fuel for bioenergetic pathways, by transactivating the gene for GLS2, a mitochondrial glutaminase that converts glutamine to glutamate (Hu et al., 2010; Suzuki et al., 2010).”
• Signal transduction in cancer. (2015, neutral): “p53 also regulates glutaminase 2, a metabolic enzyme that controls production of glutamate, which is converted to a-ketoglutarate for mitochondrial respiration and, importantly, glutathione, a critical cellular antioxidant (Hu et al. 2010; Suzuki et al. 2010).”