SUMO teams up with ubiquitin to manage hypoxia.
Hypoxia, a condition of severe oxygen shortage, induces a transcriptional response that is important for both normal embryonic development and the growth of tumors. In this issue, Cheng et al. (2007) describe how the stability of the major transcriptional regulator of the hypoxic response, HIF1alpha, is modulated by the interplay between the ubiquitin and the SUMO conjugation systems.
Ulrich
Helle D
HD
Cancer Research UK London Research Institute, Clare Hall Laboratories, South Mimms, UK. helle.ulrich@cancer.org.uk
D000818:Animals; D015687:Cell Hypoxia; D003546:Cysteine Endopeptidases; D010450:Endopeptidases / Q000172:deficiency / Q000378:metabolism*; D004921:Erythropoietin / Q000096:biosynthesis / Q000235:genetics; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism*; D051379:Mice; D011485:Protein Binding; D025801:Ubiquitin / Q000378:metabolism*; D051794:Von Hippel-Lindau Tumor Suppressor Protein / Q000378:metabolism
D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D025801:Ubiquitin; D004921:Erythropoietin; D051794:Von Hippel-Lindau Tumor Suppressor Protein; D010450:Endopeptidases; D003546:Cysteine Endopeptidases; C501974:Senp1 protein, mouse