The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Eag1 Expression Interferes with Hypoxia Homeostasis and Induces Angiogenesis in Tumors
Open accessAbstract
Ether-á-go-go-1 (Eag1) is a CNS-localized voltage-gated potassium channel that is found ectopically expressed in a majority of extracranial solid tumors. While circumstantial evidence linking Eag1 to tumor biology has been well established, the mechanisms by which the channel contributes to tumor progression remain elusive. In this study, we have used in vivo and in vitro techniques to identify a candidate mechanism. A mutation that eliminates ion permeation fails to completely abolish xenograft tumor formation by transfected cells, indicating that Eag1 contributes to tumor progression independently of its primary function as an ion channel. Our data suggest that Eag1 interferes with the cellular mechanism for maintaining oxygen homeostasis, increasing HIF-1 activity, and thereby VEGF secretion and tumor vascularization.
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Cites
Jaakkola, P., Mole, D. R., Tian, Y.-M., Wilson, M. I., Gielbert, J., Gaskell, S. J., Kriegsheim, A. V., Hebestreit, H. F., Mukherji, M., Schofield, C. J., et al. (2001) · Science · doi:10.1126/science.1059796 · Cited by 5,535
The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis
Maxwell, P. H., Wiesener, M. S., Chang, G.-W., Clifford, S. C., Vaux, E. C., Cockman, M. E., Wykoff, C. C., Pugh, C. W., Maher, E. R., & Ratcliffe, P. J. (1999) · Nature · doi:10.1038/20459 · Cited by 5,180
HIFα Targeted for VHL-Mediated Destruction by Proline Hydroxylation: Implications for O 2 Sensing
Ivan, M., Kondo, K., Yang, H., Kim, W., Valiando, J., Ohh, M., Salic, A., Asara, J. M., Lane, W. S., & Kaelin Jr., W. G. (2001) · Science · doi:10.1126/science.1059817 · Cited by 4,735
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Hypoxia signalling in cancer and approaches to enforce tumour regression
Pouysségur, J., Dayan, F., & Mazure, N. M. (2006) · Nature · doi:10.1038/nature04871 · Cited by 1,676
Molecular basis of the VHL hereditary cancer syndrome
Kaelin, W. G. (2002) · Nature Reviews Cancer · doi:10.1038/nrc885 · Cited by 865
Potassium Channels, Proliferation and G1 Progression
Wonderlin, W. F., & Strobl, J. S. (1996) · Journal of Membrane Biology · doi:10.1007/s002329900135 · Cited by 402
Cited by
Voltage-gated potassium channels as therapeutic targets
Wulff, H., Castle, N. A., & Pardo, L. A. (2009) · Nature Reviews Drug Discovery · doi:10.1038/nrd2983 · Cited by 799
Self-citationIon Channels in Cancer: Are Cancer Hallmarks Oncochannelopathies?
Prevarskaya, N., Skryma, R., & Shuba, Y. (2018) · Physiological Reviews · doi:10.1152/physrev.00044.2016 · Cited by 484
The roles of K+ channels in cancer
Pardo, L. A., & Stühmer, W. (2014) · Nature Reviews Cancer · doi:10.1038/nrc3635 · Cited by 477
Self-citationIon channels and the hallmarks of cancer
Prevarskaya, N., Skryma, R., & Shuba, Y. (2010) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2010.01.005 · Cited by 448
Potassium channels in cell cycle and cell proliferation
Urrego, D., Tomczak, A. P., Zahed, F., Stühmer, W., & Pardo, L. A. (2014) · Philosophical Transactions of the Royal Society B: Biological Sciences · doi:10.1098/rstb.2013.0094 · Cited by 388
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Metadata
- Authors
- Downie, B. R., Sánchez, A., Knötgen, H., Contreras-Jurado, C., Gymnopoulos, M., Weber, C., Stühmer, W., & Pardo, L. A.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2008-12
- Volume
- 283
- Issue
- 52
- Pages
- 36234-36240
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1992562665
- Cited by
- 175
- References
- 7
- FWCI
- 2.43
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Downie, B. R., Sánchez, A., Knötgen, H., Contreras-Jurado, C., Gymnopoulos, M., Weber, C., Stühmer, W., & Pardo, L. A. (2008). Eag1 Expression Interferes with Hypoxia Homeostasis and Induces Angiogenesis in Tumors. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m801830200
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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