TIGAR, a p53-inducible regulator of glycolysis and apoptosis.

By K. Bensaad, A. Tsuruta, M. Selak, M. N. C. Vidal, K. Nakano, R. Bartrons, Eyal Gottlieb, Karen H. Vousden. Cell, 2006

2,038 citations recorded by the source corpus.

Subfields: Biotechnology, Cancer Research, Oncology

View Paper: https://www.semanticscholar.org/paper/da8944fa0911346671bae44fc5382eae4dd4e4be

How researchers see this paper

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

In Biotechnology

1. Guido Kroemer
2. Navdeep S. Chandel
3. Karen H. Vousden
4. C. V. Dang
5. W. Gu
6. Arnold J. Levine
7. Carol Prives
8. Douglas R. Green

In Cancer Research

1. C. V. Dang
2. Navdeep S. Chandel
3. Ralph J. Deberardinis
4. Craig B. Thompson
5. Huafeng Zhang
6. Guido Kroemer
7. Jie Zheng
8. David M. Sabatini

In Oncology

1. Guido Kroemer
2. W. Gu
3. Karen H. Vousden
4. David M. Sabatini
5. Carol Prives
6. L. Galluzzi
7. Huafeng Zhang
8. Zhaoyong Li

Citations in the corpus

• Redox Regulation of Cell Survival (2008, positive): “Furthermore, a recent report showed that the p53 tumor suppressor also affects cellular redox homeostasis by inhibiting glycolysis and stimulating mitochondrial bioenergetics through transcriptional activation of TIGAR (TP53-induced glycolysis and apoptosis regulator) and the SCO2 (synthesis of cyto”
• Metabolic reprogramming and cancer progression (2020, background): “In the case of the classical tumor suppressor gene TP53, germline mutations result in a somewhat different tissue distribution of cancers than sporadic TP53-mutant cancers in patients who lack germline mutations (7).”
• The return of metabolism: biochemistry and physiology of the pentose phosphate pathway (2014, background): “…a tumour suppressor with well-established functions on genomic integrity, apoptosis and cell cycle control (Vazquez et al., 2008). p53 is the most commonly mutated gene in human cancers and its loss constitutes a pivotal mechanism of therapy failure (Bensaad et al., 2006; Rohwer et al., 2010).”
• ROS Generation and Antioxidant Defense Systems in Normal and Malignant Cells (2019, background): “TIGAR negatively regulates glycolysis and decreases intracellular ROS levels [229], while aldehyde dehydrogenase 4 (ALDH4) is a NAD+-dependent enzyme that catalyzes the second step of the proline degradation pathway in the mitochondrial matrix [230].”
• Regulation of cancer cell metabolism (2011, background): “However, p53 inhibits the glycolytic pathway by upregulating the expression of TP53-induced glycolysis and apoptosis regulator (TIGAR), an enzyme that decreases the levels of the glycolytic activator fructose-2,6-bisphosphat”
• Mitochondria in cancer cells: what is so special about them? (2008, positive): “Expression of TIGAR lowered fructose-2,6-bisphosphate levels in cells, resulting in the inhibition of glycolysis, while stimulating NADPH generation through the pentose phosphate shunt [ 30 ].”