Contrasting Properties of Hypoxia-Inducible Factor 1 (HIF-1) and HIF-2 in von Hippel-Lindau-Associated Renal Cell Carcinoma

By R. Raval, K. W. Lau, Maxine G. B. Tran, H. Sowter, S. Mandriota, Ji-Liang Li, C. Pugh, P. Maxwell, Adrian L. Harris, P. Ratcliffe. Molecular and Cellular Biology, 2005

993 citations recorded by the source corpus.

Subfields: Cancer Research, Surgery

View Paper: https://www.semanticscholar.org/paper/ea22eef976a8498d9b440e9cf543425e3baaa66d

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In Cancer Research

1. G. Semenza
2. C. V. Dang
3. M. C. Simon
4. W. Kaelin
5. P. Ratcliffe
6. B. Keith
7. Jeremy N. Rich
8. Ping Gao

In Surgery

1. G. Semenza
2. W. Kaelin
3. M. C. Simon
4. C. V. Dang
5. Quynh-Thu Le
6. Erinn B. Rankin
7. Michael Story
8. K. Ang

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 spite of these significant similarities in their DNA binding and dimerization domains, we and others demonstrated that HIF-1 and HIF-2 have unique as well as common target genes when endogenous HIF target genes were analyzed (Hu et al., 2003; Grabmaier et al., 2004; Warnecke et al., 2004; Raval e”
• The von Hippel–Lindau tumour suppressor protein: O2 sensing and cancer (2008, background): “Second, overproduction of HIF2α (for example, using a stabilized version of HIF2α lacking its prolyl hydroxylation sites), but not HIF1α, is sufficient to override the tumour suppressor function of VHL in xenograft studie”
• HIF-1 inhibits mitochondrial biogenesis and cellular respiration in VHL-deficient renal cell carcinoma by repression of C-MYC activity. (2007, background): “HIF-1 heterodimers containing HIF-1 a or HIF-2 a regulate an overlapping but distinct set of transcriptional target genes (Hu et al., 2003; Raval et al., 2005).”
• Hypoxia inducible mir-210 regulates normoxic gene expression involved in tumor initiation (2009, positive): “This was a surprising result because HIF1a is generally considered a promoter of tumorigenesis, although some published data suggest it can also inhibit tumor growth (Carmeliet et al., 1998; Maranchie et al., 2002; Raval et al., 2005).”
• The role of hypoxia-inducible factors in tumorigenesis (2008, background): “Renal + + HIF-1 positive Raval et al.(66)”
• Hypoxia-Inducible Factors Regulate Tumorigenic Capacity of Glioma Stem Cells (2009, positive): “Because HIF1a is universally expressed while HIF2a shows a more restricted expression pattern, relatively few studies have determined the role of HIF2a in cancer initiation or tumor progression (Covello et al., 2006; Holmquist-Mengelbier et al., 2006; Hu et al., 2006; Raval et al., 2005).”
• HIF-2alpha regulates Oct-4: effects of hypoxia on stem cell function, embryonic development, and tumor growth. (2006, background): “Several experiments have shown that expression of HIF-2 promotes more rapid growth of RCC xenografts (Kondo et al. 2002, 2003; Maranchie et al. 2002; Raval et al. 2005) and ES cell-derived teratomas (Covello et al.”
• The impact of O2 availability on human cancer (2008, background): “Similarly, HIF1α expression gradually decreases whereas HIF2α expression increases as renal carcinomas develop in patients with VHL disease, the cancer susceptibility syndrome that is associated with germline VHL mutation”
• Oxygen sensing by metazoans: the central role of the HIF hydroxylase pathway. (2008, background): “Studies of transcriptional selectivity have defined exclusive HIF1a targets, exclusive HIF2a targets, and genes that are responsive to both HIF1a and HIF2a (Holmquist-Mengelbier et al., 2006; Hu et al., 2003; Raval et al., 2005).”
• ADAPTIVE AND MALADAPTIVE CARDIORESPIRATORY RESPONSES TO CONTINUOUS AND INTERMITTENT HYPOXIA MEDIATED BY HYPOXIA-INDUCIBLE FACTORS 1 AND 2 (2012, background): “Some HIF-1 target genes, such as EPO, GLUT1, VEGF, and EGLN3, can be activated by either HIF-1 or HIF-2, whereas other target genes, such as BNIP3, CAR9, LDHA, and PGK1, are only activated by HIF-1 (78, 123, 275, 318).”
• Hypoxia promotes expansion of the CD133-positive glioma stem cells through activation of HIF-1α (2009, background): “These data suggest that inhibition of the growth factor signaling pathway may attenuate hypoxia-induced expansion of CD133-positive CSCs. Oncogene Propagation at hypoxia expands the CD133/CXCR4/ CD44low/A2B5/CD24-positive cells To further characterize the phenotype of the CSC subpopulation showing e”