Prolyl hydroxylase-1 negatively regulates IκB kinase-β, giving insight into hypoxia-induced NFκB activity

By E. Cummins, E. Berra, Katrina M. Comerford, A. Ginouvès, Kathleen T. Fitzgerald, Fergal Seeballuck, C. Godson, Jens Erik Nielsen, P. Moynagh, J. Pouysségur and 1 more. Proceedings of the National Academy of Sciences of the United States of America, 2006

706 citations recorded by the source corpus.

Subfields: Biochemistry, Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/bca643294a8572cde2857b31d4cd5f88bee83cc9

How researchers see this paper

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In Biochemistry

1. W. Kaelin

In Cancer Research

1. W. Kaelin
2. P. Ratcliffe
3. V. Nizet
4. A. Palazón
5. Richard J. Johnson
6. Ananda W. Goldrath
7. G. Semenza
8. M. C. Simon

In Molecular Biology

1. P. Ratcliffe
2. W. Kaelin
3. Richard J. Johnson
4. G. Semenza
5. M. C. Simon

Citations in the corpus

• HIF Transcription Factors, Inflammation, and Immunity (2014, background): “As noted above, hypoxia and bacterial infections result in increased nuclear factor-kappa B (NF-kB) activity in phagocytes, which in turn induces HIF-1a mRNA transcription (Cummins et al., 2006; Fitzpatrick et al., 2011; Rius et al., 2008).”
• Oxygen sensing by metazoans: the central role of the HIF hydroxylase pathway. (2008, positive): “IKKb contains a colinear sequence that resembles the prolyl hydroxylation sites in HIFa although it has not yet been proven that this site is hydroxylated.”