Regulation of Hypoxia-Inducible mRNAs by the von Hippel-Lindau Tumor Suppressor Protein Requires Binding to Complexes Containing Elongins B/C and Cul2 | Zendy

Kim M. Lonergan | Zendy; Othon Iliopoulos | Zendy; Michael Ohh | Zendy; Takumi Kamura | Zendy; Ronald Conaway | Zendy; Joan Conaway | Zendy; William G. Kaelin | Zendy

Open Access

Regulation of Hypoxia-Inducible mRNAs by the von Hippel-Lindau Tumor Suppressor Protein Requires Binding to Complexes Containing Elongins B/C and Cul2

Author(s) -

Kim M. Lonergan,

Othon Iliopoulos,

Michael Ohh,

Takumi Kamura,

Ronald Conaway,

Joan Conaway,

William G. Kaelin

Publication year - 1998

Publication title -

molecular and cellular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.14

H-Index - 327

eISSN - 1067-8824

pISSN - 0270-7306

DOI - 10.1128/mcb.18.2.732

Subject(s) - biology , suppressor , microbiology and biotechnology , hypoxia inducible factor 1 , hypoxia (environmental) , tumor suppressor gene , gene , cancer research , genetics , transcription factor , carcinogenesis , chemistry , organic chemistry , oxygen

The von Hippel-Lindau tumor suppressor protein (pVHL) binds to elongins B and C and posttranscriptionally regulates the accumulation of hypoxia-inducible mRNAs under normoxic (21% O2) conditions. Here we report that pVHL binds, via elongin C, to the human homolog of the Caenorhabditis elegans Cul2 protein. Coimmunoprecipitation and chromatographic copurification data suggest that pVHL-Cul2 complexes exist in native cells. pVHL mutants that were unable to bind to complexes containing elongin C and Cul2 were likewise unable to inhibit the accumulation of hypoxia-inducible mRNAs. A model for the regulation of hypoxia-inducible mRNAs by pVHL is presented based on the apparent similarity of elongin C and Cul2 to Skp1 and Cdc53, respectively. These latter proteins form complexes that target specific proteins for ubiquitin-dependent proteolysis.

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