An intact NEDD8 pathway is required for Cullin‐dependent ubiquitylation in mammalian cells
Open Access
- 1 February 2002
- journal article
- research article
- Published by Springer Nature in EMBO Reports
- Vol. 3 (2) , 177-182
- https://doi.org/10.1093/embo-reports/kvf028
Abstract
Skp1‐Cdc53/Cul1‐F‐box (SCF) complexes constitute a class of E3 ubiquitin ligases. Recently, a multiprotein complex containing pVHL, elongin C and Cul2 (VEC) was shown to structurally and functionally resemble SCF complexes. Cdc53 and the Cullins can become covalently linked to the ubiquitin‐like molecule Rub1/NEDD8. Inhibition of neddylation inhibits SCF function in vitro and in yeast and plants. Here we show that ongoing neddylation is likewise required for VEC function in vitro and for the degradation of SCF and VEC targets in mammalian cells. Thus, neddylation regulates the activity of two specific subclasses of mammalian ubiquitin ligases.Keywords
This publication has 41 references indexed in Scilit:
- A new NEDD8-ligating system for cullin-4AGenes & Development, 1998
- A novel protein modification pathway related to the ubiquitin systemThe EMBO Journal, 1998
- Modification of yeast Cdc53p by the ubiquitin-related protein Rub1p affects function of the SCFCdc4 complexGenes & Development, 1998
- Regulation of Hypoxia-Inducible mRNAs by the von Hippel-Lindau Tumor Suppressor Protein Requires Binding to Complexes Containing Elongins B/C and Cul2Molecular and Cellular Biology, 1998
- The von Hippel-Lindau tumor-suppressor gene product forms a stable complex with human CUL-2, a member of the Cdc53 family of proteinsProceedings of the National Academy of Sciences, 1997
- Dominant-negative cyclin-selective ubiquitin carrier protein E2-C/UbcH10 blocks cells in metaphaseProceedings of the National Academy of Sciences, 1997
- Binding of the von Hippel-Lindau Tumor Suppressor Protein to Elongin B and CScience, 1995
- Tumour suppression by the human von Hippel-Lindau gene productNature Medicine, 1995
- The ts41 mutation in Chinese hamster cells leads to successive S phases in the absence of intervening G2, M, and G1Cell, 1992
- Isolation by a replica‐plating technique of chinese hamster temperature‐sensitive cell cycle mutantsJournal of Cellular Physiology, 1982