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Inactivation of the...
Inactivation of the CYLD Deubiquitinase by HPV E6 Mediates Hypoxia-Induced NF-kappa B Activation
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An, Jiabin (author)
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Mo, Deqiong (author)
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Liu, Huiren (author)
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Veena, Mysore S. (author)
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Srivatsan, Eri S. (author)
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- Massoumi, Ramin (author)
- Lund University,Lunds universitet,Cellpatologi, Malmö,Forskargrupper vid Lunds universitet,Cell Pathology, Malmö,Lund University Research Groups
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Rettig, Matthew B. (author)
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(creator_code:org_t)
- Elsevier BV, 2008
- 2008
- English.
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In: Cancer Cell. - : Elsevier BV. - 1878-3686 .- 1535-6108. ; 14:5, s. 394-407
- Related links:
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http://dx.doi.org/10...
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http://www.cell.com/...
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https://lup.lub.lu.s...
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https://doi.org/10.1...
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Abstract
Subject headings
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- The biochemical mechanisms that underlie hypoxia-induced NF-kappa B activity have remained largely undefined. Here, we find that prolonged hypoxia-induced NF-kappa B activation is restricted to cancer cell lines infected with high-risk human papillomavirus (HPV) serotypes. The HPV-encoded E6 protein is necessary and sufficient for prolonged hypoxia-induced NF-kappa B activation in these systems. The molecular target of E6 in the NF-kappa B pathway is the CYLD lysine 63 (K63) deubiquitinase, a negative regulator of the NF-kappa B pathway. Specifically, hypoxia stimulates E6-mediated ubiquitination and proteasomal degradation of CYLD. Given the established role of NF-kappa B in human carcinogenesis, these findings provide a potential molecular/viral link between hypoxia and the adverse clinical outcomes observed in HPV-associated malignancies.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Cancer och onkologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Cancer and Oncology (hsv//eng)
Publication and Content Type
- art (subject category)
- ref (subject category)
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