Cellular adaptation to hypoxia: O2‐sensing protein hydroxylases, hypoxia‐inducible transcription factors, and O2‐regulated gene expression

By Roland H. Wenger. The FASEB Journal, 2002

1,265 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/3b973635dd9e569aa3943c65de2bf781d95e80d3

How researchers see this paper

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In Cancer Research

1. P. Schumacker
2. M. C. Simon
3. R. Guzy
4. B. Keith
5. Cheng-Jun Hu
6. P. Thomas
7. Liyi Wang
8. Yi Pan

In Molecular Biology

1. P. Schumacker
2. M. C. Simon
3. R. Guzy
4. B. Keith
5. Cheng-Jun Hu
6. P. Thomas
7. M. Hartnett
8. Liyi Wang

In Physiology

1. M. C. Simon
2. I. Wood
3. P. Trayhurn
4. Cheng-Jun Hu
5. B. Keith
6. P. Thomas
7. Liyi Wang
8. Yi Pan

Citations in the corpus

• Differential Roles of Hypoxia-Inducible Factor 1α (HIF-1α) and HIF-2α in Hypoxic Gene Regulation (2003, positive): “Both HIF-1 and HIF-2 have been implicated in hypoxia responses (19, 106).”
• Mitochondrial dysfunction resulting from loss of cytochrome c impairs cellular oxygen sensing and hypoxic HIF-alpha activation. (2005, positive): “Hypoxia inhibits hydroxylation and stabilized HIF-α translocates to the nucleus, dimerizes with a HIF-β subunit (ARNT) and activates transcription (Bruick, 2003; Wenger, 2002).”
• Endothelial cell superoxide generation: regulation and relevance for cardiovascular pathophysiology. (2004, background): “Chronic changes in cellular function in many tissues, including the endothelium, involve redox-sensitive activation of the transcription factor hypoxia-inducible factor-1 (HIF-1), which may increase the expression of genes involved in angiogenesis, energy metabolism, cell proliferation, and vascular”
• Mitochondrial Glutathione, a Key Survival Antioxidant (2009, background): “Hypoxia occurs in tissues when the availability of O2 is insufficient for the cellular demand, as happens in physiologic (embryonic development, exercising muscle) and pathologic conditions (stroke, tissue ischemia, inflammation, solid-tumor formation) (6, 116, 126, 132, 143).”
• Hypoxia-Inducible Factor-1 (HIF-1) (2006, neutral): “zymes and glucose transporters (Wenger, 2002).”
• Vascular endothelial growth factor in eye disease. (2008, background): “When this occurs, HIF-1α complexes with HIF-1β, translocates into the nucleus and binds to a specific sequence in the 5′ flanking region of the VEGF gene, the hypoxia responsive element (HRE) (Ikeda et al., 1995; Laughner et al., 2001; Shima et al., 1996; Wenger, 2002; Forsythe et al., 1996).”
• Biomarkers of hypoxia exposure and reproductive function in Atlantic croaker: a review with some preliminary findings from the northern Gulf of Mexico hypoxic zone. (2009, background): “Both HIF α and β subunits are members of the basic helix–loop–helix (bHLH) family of transcription factors containing the Per-ARNT-Sim (PAS) domains (Wang et al., 1995; Wenger, 2002).”
• Adipokines: inflammation and the pleiotropic role of white adipose tissue (2004, background): “Hypoxia is characteristic of tumours, where HIF-1 expression is increased, as well as in other disorders such as ischaemic heart disease (Binley et al. 2003; Höpfl et al. 2004).”
• HIF‐1α induces cell cycle arrest by functionally counteracting Myc (2004, background): “It appears that HIF-1a, a basic helix–loop–helix (bHLH) transcription factor of the PAS family (Wang et al, 1995), is responsible for upregulating most, if not all, hypox- ia-inducible genes (Semenza, 1999; Wenger, 2002).”