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Cullin 3, the core subunit of the CRL3 ubiquitin ligase family, is essential for development, but its substrates remain poorly defined. Here, Chen et al. (2009) report that CRL3(BACURD) targets the RhoA GTPase for degradation, thereby maintaining actin cytoskeleton integrity.
Chen,
Cullin mediates degradation of RhoA through evolutionarily conserved BTB adaptors to control actin cytoskeleton structure and cell movement.
2009, Pubmed,
Xenbase
Chen,
Cullin mediates degradation of RhoA through evolutionarily conserved BTB adaptors to control actin cytoskeleton structure and cell movement.
2009,
Pubmed
,
Xenbase
Geyer,
BTB/POZ domain proteins are putative substrate adaptors for cullin 3 ubiquitin ligases.
2003,
Pubmed
Jaffe,
Rho GTPases: biochemistry and biology.
2005,
Pubmed
Kobayashi,
Molecular mechanisms activating the Nrf2-Keap1 pathway of antioxidant gene regulation.
2005,
Pubmed
Loignon,
Cul3 overexpression depletes Nrf2 in breast cancer and is associated with sensitivity to carcinogens, to oxidative stress, and to chemotherapy.
2009,
Pubmed
Orlicky,
Structural basis for phosphodependent substrate selection and orientation by the SCFCdc4 ubiquitin ligase.
2003,
Pubmed
Singer,
Cullin-3 targets cyclin E for ubiquitination and controls S phase in mammalian cells.
1999,
Pubmed
Soucy,
An inhibitor of NEDD8-activating enzyme as a new approach to treat cancer.
2009,
Pubmed
Stogios,
Sequence and structural analysis of BTB domain proteins.
2005,
Pubmed
Sumara,
A Cul3-based E3 ligase removes Aurora B from mitotic chromosomes, regulating mitotic progression and completion of cytokinesis in human cells.
2007,
Pubmed
Tang,
Suprafacial orientation of the SCFCdc4 dimer accommodates multiple geometries for substrate ubiquitination.
2007,
Pubmed
