Transcription Factor HIF-1 Is a Necessary Mediator of the Pasteur Effect in Mammalian Cells

By T. Seagroves, H. E. Ryan, Han Lu, Bradly G. Wouters, M. Knapp, P. Thibault, K. Laderoute, Richard J. Johnson. Molecular and Cellular Biology, 2001

628 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/9537472e8eb83ca23cc33bdf5e723d9d736e663f

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. G. Semenza
2. C. V. Dang
3. M. C. Simon
4. W. Kaelin
5. Jung-whan Kim
6. P. Ratcliffe
7. N. Denko
8. Ping Gao

In Genetics

1. G. Semenza
2. C. V. Dang
3. M. C. Simon
4. Cormac T. Taylor
5. N. Prabhakar
6. W. Kaelin
7. P. Ratcliffe
8. S. Kierans

In Molecular Biology

1. G. Semenza
2. C. V. Dang
3. W. Kaelin
4. M. C. Simon
5. Jung-whan Kim
6. P. Ratcliffe
7. N. Denko
8. Ping Gao

Citations in the corpus

• Adipocyte-derived Th2 cytokines and myeloid PPARdelta regulate macrophage polarization and insulin sensitivity. (2008, background): “On the other hand, glycolysis is known to provide the energy required to mount an inflammatory response (Cramer et al., 2003; Kim et al., 2006; Seagroves et al., 2001).”
• Contrasting Properties of Hypoxia-Inducible Factor 1 (HIF-1) and HIF-2 in von Hippel-Lindau-Associated Renal Cell Carcinoma (2005, background): “Activation of HIF in cancer has been shown to contribute to the classical tumor phenotypes of upregulated glycolysis and angiogenesis (23, 28, 34, 36), leading to widespread interest in the HIF system as a target in cancer therapeutics (37).”
• Causes and Consequences of Increased Glucose Metabolism of Cancers (2008, background): “Its centrality to the regulation of glucose metabolism has led to the general belief that it alone can be responsible for the Warburg or Pasteur effects (118,119).”
• HIF-1 regulates cytochrome oxidase subunits to optimize efficiency of respiration in hypoxic cells. (2007, positive): “Previous studies have demonstrated that HIF-1 transactivates genes encoding glucose transporters and glycolytic enzymes in response to reduced O 2 availability (Semenza et al., 1996; Iyer et al., 1998; Seagroves et al., 2001).”
• Targeting HIF-1 for cancer therapy (2003, background): “The concomitant induction of angiogenesis and glycolysis with cell proliferation is mediated partly by activating HIF-1 (Ref”
• HIF-1 inhibits mitochondrial biogenesis and cellular respiration in VHL-deficient renal cell carcinoma by repression of C-MYC activity. (2007, background): “Previous studies have demonstrated that HIF-1 transactivates genes encoding glucose transporters and glycolytic enzymes, including LDH-A, thus increasing flux through the glycolytic pathway and the conversion of pyruvate to lactate (Semenza et al., 1994, 1996; Firth et al., 1995; Iyer et al., 1998; ”
• Pyruvate Kinase M2 is a PHD3-stimulated Coactivator for Hypoxia-Inducible Factor 1 (2011, positive): “Activation of hypoxia-inducible factor 1 (HIF-1), which commonly occurs in human cancers either as a result of hypoxia or genetic alterations (Harris, 2002; Semenza, 2010), leads to a switch from oxidative to glycolytic metabolism (Seagroves et al., 2001;Wheaton andChandel, 2011).”
• Inhibition of HIF is necessary for tumor suppression by the von Hippel-Lindau protein. (2002, background): “Furthermore, it has not been shown Seagroves et al., 2001).”
• The Histone Deacetylase SIRT6 Regulates Glucose Homeostasis via Hif1α (2010, neutral): “The hypoxia-inducible transcription factor Hif1a is a key mediator of this cellular adaptation to nutrient and oxygen stress (Lum et al., 2007; Seagroves et al., 2001), functioning as a direct transcriptional activator of multiple genes.”
• MicroRNA-210 Controls Mitochondrial Metabolism during Hypoxia by Repressing the Iron-Sulfur Cluster Assembly Proteins ISCU1/2 (2009, neutral): “The elucidation of the miR-210-ISCU1/2 regulatory pathway substantially clarifies the nature of the complex crosstalk between HIF-1a and mitochondria (Seagroves et al., 2001) and complements other HIF-dependent processes proposed to regulate the mismatch of reduced oxygen tension and mitochondrial e”
• Differential Roles of Hypoxia-Inducible Factor 1α (HIF-1α) and HIF-2α in Hypoxic Gene Regulation (2003, positive): “This finding is consistent with previous data indicating that HIF-1 is necessary for glycolytic capacity in multiple cells, such as granulocytes, monocytes/ macrophages (20), chondrocytes (86), and MEFs (91).”
• Regulation of glycolysis by the hypoxia‐inducible factor (HIF): implications for cellular physiology (2020, background): “To date multiple mechanisms have been described as important regulators of glycolysis under hypoxic conditions, including those dependent on the actions of the HIF pathway (Seagroves et al. 2001), the PI3K/Akt pathway (Xie et al.”
• SIRT3 opposes reprogramming of cancer cell metabolism through HIF1α destabilization (2011, background): “SIRT3 Opposes the Warburg Effect by Destabilizing HIF1a HIF1, the heterodimer of HIF1a andHIF1b, is the primary driver of increased glycolysis and lactate production during hypoxia (Gordan and Simon, 2007; Hu et al., 2003; Seagroves et al., 2001).”
• Hypoxia — a key regulatory factor in tumour growth (2002, background): “Hypoxic cancer cells use glycolysis as a primary mechanism of ATP production, and cellular transformation has been associated with induction of glycolysi”