Hypoxia requires notch signaling to maintain the undifferentiated cell state.

By M. Gustafsson, Xiaowei Zheng, T. Pereira, K. Gradin, Shaobo Jin, J. Lundkvist, J. Ruas, L. Poellinger, U. Lendahl, M. Bondesson. Developmental Cell, 2005

1,170 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/9722be7764d8de9499ed751932e894b4697ca6e6

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. M. C. Simon
3. W. Kaelin
4. P. Ratcliffe
5. B. Keith
6. V. Haase
7. Amato J. Giaccia
8. Richard J. Johnson

In Molecular Biology

1. G. Semenza
2. M. C. Simon
3. W. Kaelin
4. P. Ratcliffe
5. S. Påhlman
6. C. Wigerup
7. D. Bexell
8. B. Keith

Citations in the corpus

• Oxygen sensing by metazoans: the central role of the HIF hydroxylase pathway. (2008, background): “To date, however, the functional significance of FIH1-mediated hydroxylation of IkBs and Notch receptors is unclear.”
• Hypoxia promotes expansion of the CD133-positive glioma stem cells through activation of HIF-1α (2009, background): “Recent studies implicate oxygen tension as a key regulator of the NSC metabolic state, survival and fate (Gustafsson et al., 2005; Chen et al., 2007).”
• Hypoxia-induced angiogenesis: good and evil. (2011, background): “HIF-1α directly binds to the Notch intracellular domain (NICD) and augments its transcriptional activity.(62) Additionally, the Notch ligand Dll4 is a transcriptional target of both HIF-1α and HIF-2α in the endothelium.”
• Mechanisms of disease: pulmonary arterial hypertension (2011, background): “90 Notch 3 also regulates expression of PDGF receptor β in vascular SMCs.”
• Signaling mechanisms of the epithelial-mesenchymal transition (2014, background): “Not only does HIF-1α stimulate Notch signaling, but it also stabilizes nuclear NICD, which is involved in the induction of many EMT-associated genes (246, 247).”
• ADAPTIVE AND MALADAPTIVE CARDIORESPIRATORY RESPONSES TO CONTINUOUS AND INTERMITTENT HYPOXIA MEDIATED BY HYPOXIA-INDUCIBLE FACTORS 1 AND 2 (2012, background): “In other cases, HIF-1 binds to transcription factors and enhances their transactivation function (106).”
• Therapeutic targeting of hypoxia and hypoxia-inducible factors in cancer. (2016, background): “The stem cell-like state ismediated by upregulation of OCT4, Notch, c-Myc, and telomerase (Keith & Simon, 2007).”
• Hypoxia promotes fibrogenesis in vivo via HIF-1 stimulation of epithelial-to-mesenchymal transition. (2007, background): “However, the molecular events underlying EMT are complex, and because of the transcriptional pleiotropism of HIF-1 and the ability of its α subunit to interact with non-PAS domain proteins, its role in EMT via modulation of other molecular pathways, such as the Notch (48) or TGF-β signaling pathways”
• The role of hypoxia-inducible factors in tumorigenesis (2008, background): “Hypoxia has been shown to prevent the differentiation of progenitor cells and promote dedifferentiation of cancer cells.86–89 Gustafsson et al.86 has provided evidence to suggest that Notch plays an important role in maintaining a dedifferentiated state under hypoxia in multiple cell types, includin”
• Bmi1 is essential in Twist1-induced epithelial–mesenchymal transition (2010, background): “Previous research has demonstrated that HIF-1α activates the Notch pathwa”
• Hypoxia-inducible factors in stem cells and cancer (2009, neutral): “However, a role for HIF’s activation of Notch target genes were only partially investigated: exactly how HIF-1 proteins integrate into the Notch ICD:MAML:CSL complex is not yet understood, nor is it known whether this response modulates the expression of all Notch target genes, or only a subset [55]”