Hypoxia-inducible factor 1: oxygen homeostasis and disease pathophysiology.

By G. Semenza. Trends in Molecular Medicine, 2001

959 citations recorded by the source corpus.

Subfields: Cancer Research, Genetics, Physiology

View Paper: https://www.semanticscholar.org/paper/4159e9c6cabca08b8f6dcc7ef451859874c455d4

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. M. C. Simon
2. P. Ratcliffe
3. B. Keith
4. G. Semenza
5. A. Mantovani
6. Christopher J. Schofield
7. Cheng-Jun Hu
8. A. Sica

In Genetics

1. M. C. Simon
2. B. Keith
3. Christopher J. Schofield
4. U. Lendahl
5. P. Ratcliffe
6. G. Semenza

In Physiology

1. M. C. Simon
2. P. Ratcliffe
3. Cheng-Jun Hu
4. A. Sica
5. B. Keith
6. Christopher J. Schofield
7. Liyi Wang
8. A. Mantovani

Citations in the corpus

• The N-Terminal Transactivation Domain Confers Target Gene Specificity of Hypoxia-inducible Factors HIF-1α and HIF-2α (2007, background): “In response to hypoxic stress, mammalian cells activate hypoxia-inducible transcription factors (HIFs) to enhance the transcription of genes involved in glycolysis, angiogenesis, and cell survival to maintain oxygen homeostasis (Semenza, 2001).”
• Oxygen sensing by HIF hydroxylases (2004, background): “The HIFα/β dimer binds to a core DNA motif (G/ACGTG) in hypoxia-response elements (HREs) that are associated with a broad range of transcriptional targets (for reviews, see Ref”
• Permeability Studies on In Vitro Blood–Brain Barrier Models: Physiology, Pathology, and Pharmacology (2005, background): “Among hypoxia-inducible factor 1 regulated genes (Semenza, 2001), endothelin-1, inducible NO synthase (iNOS), TGF-β, and VEGF contribute to the damage of BBB integrity, whereas adrenomedullin reinforces the barrier function (Tables IV, VII, and X).”
• Notch signaling mediates hypoxia-induced tumor cell migration and invasion (2008, background): “When stabilized in hypoxia, HIF-1 dimerizes with HIF-1 (ARNT) and activates downstream genes involved in the canonical hypoxic response via HRE elements in their promoters (15, 16).”
• The hypoxia-inducible factor alpha pathway couples angiogenesis to osteogenesis during skeletal development. (2007, neutral): “, angiogenesis) to reduced oxygen availability (3).”
• Regulation of the Chemokine Receptor CXCR4 by Hypoxia (2003, background): “VEGF gene expression is induced by Hyp (1) and served as an internal control.”
• The role of oxygen availability in embryonic development and stem cell function (2008, background): “Hypoxia is commonly associated with pathologies such as tissue ischaemia and inflammation, and occurs in solid tumour”
• Structural basis for negative regulation of hypoxia-inducible factor-1α by CITED2 (2003, background): “Not surprisingly, therefore, HIF-1 is implicated in the pathogenesis of some cancers and in the recovery from myocardial and cerebral ischemi”
• Binding of Natively Unfolded HIF-1α ODD Domain to p53 (2005, neutral): “Diverse evidence suggests that hypoxia survival (Semenza, 2001).”