The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
Hypoxia rapidly activates HIF‐3α mRNA expression
Abstract
The role of the hypoxia‐inducible factor (HIF) subunits 1α and 1β in cellular response to hypoxia is well established, whereas little is known about HIF‐2α and HIF‐3α with respect to organ distribution and transcriptional regulation by hypoxia. We investigated mRNA levels of all HIF subunits and of their target genes erythropoietin (EPO) and glucose‐transporter 1 (GLUT1) in rats undergoing systemic hypoxia for 30 or 120 min by quantitative real‐time RT‐PCR. In normoxia, persistently high mRNA levels of all HIF subunits were detected in cerebral cortex, hippocampus, and lung; the heart contained the lowest amounts. Hypoxia did not affect mRNA levels of HIF‐1α, ‐1β, and ‐2α. HIF‐3α mRNA levels increased in all organs examined after 2 h of hypoxia. A significant rise of EPO and GLUT1 mRNA levels occurred in cortex, heart, liver, and kidney after 2 h of hypoxia, indicating activation of the HIF system. Protein levels of all HIF subunits, determined in brain and lung by immunoblotting, showed a marked increase corresponding to the duration of hypoxia. Our results suggest that induction at the transcriptional level is a unique feature of HIF‐3α, which therefore may represent a rapidly reacting component of the HIF system in protection against hypoxic damage.
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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 · cited 1×
“An oxygen-dependent degradation domain (ODD) of HIF-1α has been discovered (14), which has been found to be regulated by the hydroxylation of two proline residues, requiring oxygen and Fe for its activity (15, 16).”
BackgroundActivation of vascular endothelial growth factor gene transcription by hypoxia-inducible factor 1
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Inhibitory PAS domain protein is a negative regulator of hypoxia-inducible gene expression
Makino, Y., Cao, R., Svensson, K., Bertilsson, G., Asman, M., Tanaka, H., Cao, Y., Berkenstam, A., & Poellinger, L. (2001) · Nature · doi:10.1038/35107085 · Cited by 705
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Cancer Cell Metabolism in Hypoxia: Role of HIF-1 as Key Regulator and Therapeutic Target
Infantino, V., Santarsiero, A., Convertini, P., Todisco, S., & Iacobazzi, V. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22115703 · Cited by 499
Uchida, T., Rossignol, F., Matthay, M. A., Mounier, R., Couette, S., Clottes, E., & Clerici, C. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m400461200 · Cited by 428
Reactive oxygen species in the control of hypoxia-inducible factor-mediated gene expression
Kietzmann, T., & Görlach, A. (2005) · Seminars in Cell & Developmental Biology · doi:10.1016/j.semcdb.2005.03.010 · Cited by 295
Hypoxia-inducible factor 3 biology: complexities and emerging themes
Duan, C. (2016) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00315.2015 · Cited by 269
Beyond oxygen: complex regulation and activity of hypoxia inducible factors in pregnancy
Pringle, K. G., Kind, K. L., Sferruzzi-Perri, A. N., Thompson, J. G., & Roberts, C. T. (2010) · Human Reproduction Update · doi:10.1093/humupd/dmp046 · Cited by 259
Metadata
- Authors
- Heidbreder, M., Fröhlich, F., Jöhren, O., Dendorfer, A., Qadri, F., & Dominiak, P.
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2003-06-03
- Volume
- 17
- Issue
- 11
- Pages
- 1-19
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W2128749280
- Cited by
- 182
- References
- 8
- FWCI
- 3.12
- Type
- journal article
- Language
- en
- Open access
- closed
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