Mechanism of regulation of the hypoxia‐inducible factor‐1α by the von Hippel‐Lindau tumor suppressor protein

By Keiji Tanimoto, Y. Makino, T. Pereira, L. Poellinger. EMBO Journal, 2000

938 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/c7b9e0d79ae22c2040abfd74abbcdca8d11c0d47

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In Cancer Research

1. G. Semenza
2. W. Kaelin
3. P. Schumacker
4. Adrian L. Harris
5. R. Guzy
6. J. Espinosa
7. V. L. Dengler
8. M. Galbraith

In Molecular Biology

1. G. Semenza
2. W. Kaelin
3. P. Schumacker
4. Adrian L. Harris
5. J. Espinosa
6. V. L. Dengler
7. M. Galbraith
8. R. Guzy

In Oncology

1. G. Semenza
2. W. Kaelin
3. Adrian L. Harris
4. J. Espinosa
5. V. L. Dengler
6. M. Galbraith
7. P. Vaupel
8. P. Ney

Citations in the corpus

• HIF‐1α induces cell cycle arrest by functionally counteracting Myc (2004, background): “…of HIF-1a is mediated by the von Hippel-Lindau tumor suppressor (Maxwell et al, 1999; Cockman et al, 2000; Kamura et al, 2000; Ohh et al, 2000; Tanimoto et al, 2000), a part of an E3 ubiquitin ligase, that binds to the oxygen-dependent degrada- tion domain (ODD) (Huang et al, 1998; Huang and…”
• Molecular basis of the VHL hereditary cancer syndrome (2002, background): “On the basis of this lead, several groups went on to show that the pVHL β-domain binds directly to the HIF-α subunits and that pVHL is indeed capable of directing the polyubiquitylation, and hence destruction, of the HIF-α subunit”
• Contrasting Properties of Hypoxia-Inducible Factor 1 (HIF-1) and HIF-2 in von Hippel-Lindau-Associated Renal Cell Carcinoma (2005, neutral): “The positive interaction observed with overexpression in RCC4/VHL but not RCC4 cells indicates that the change in behavior is determined not by cell background but by the presence of an intact VHL degradation pathway and is consistent with previous data indicating that this pathway can be readily sa”
• Inhibitory PAS domain protein is a negative regulator of hypoxia-inducible gene expression (2001, methodology): “pcDNA3 IPAS was constructed by insertion of an Eco RI– Not I fragment from pT7T3D IPAS (GenBank AA028416) into pcDNA3 (Invitrogen), and this vector was used to subclone IPAS into the pCMV Flag vecto”
• Oxygen sensing by mitochondria at complex III: the paradox of increased reactive oxygen species during hypoxia (2006, background): “Prolyl hydroxylases (PH) are a family of mixed function oxidases involved in the post-translational modification that signals HIF-α for degradation (Tanimoto et al. 2000; Clifton et al. 2001; Epstein et al. 2001; Bruick & McKnight, 2001; Berra et al. 2003; Appelhoff et al. 2004).”
• FIH-1 is an asparaginyl hydroxylase enzyme that regulates the transcriptional activity of hypoxia-inducible factor. (2002, background): “…ligase complex that targets the alpha subunit for degradation by the proteasome (Maxwell et al. 1999; Cockman et al. 2000; Ohh et al. 2000; Tanimoto et al. 2000). pVHL recognition of HIF- is dependent on hydroxylation of proline residues within the ODD (Ivan et al. 2001; Jaakkola et al.…”