Molecular pathogenesis of the von Hippel-Lindau hereditary cancer syndrome: implications for oxygen sensing

Cell Growth Differ. 2001 Sep;12(9):447-55.

Authors

H Yang¹, W G Kaelin Jr

Affiliation

¹ Dana-Farber Cancer Institute and Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

PMID: 11571227

No abstract available

Publication types

Review

MeSH terms

Animals
Cell Cycle
Cell Cycle Proteins / metabolism
Cullin Proteins*
Disease Models, Animal
Elongin
Extracellular Matrix / metabolism
Genotype
Humans
Hypoxia
Ligases / genetics
Ligases / metabolism*
Neoplasms / physiopathology
Oxygen / metabolism*
Phenotype
Protein Processing, Post-Translational
Transcription Factors / metabolism
Tumor Suppressor Proteins*
Ubiquitin-Protein Ligases*
Ubiquitins / metabolism
Von Hippel-Lindau Tumor Suppressor Protein
von Hippel-Lindau Disease / genetics
von Hippel-Lindau Disease / metabolism*
von Hippel-Lindau Disease / physiopathology

Substances

CUL2 protein, human
Cell Cycle Proteins
Cullin Proteins
Elongin
Transcription Factors
Tumor Suppressor Proteins
Ubiquitins
Ubiquitin-Protein Ligases
Von Hippel-Lindau Tumor Suppressor Protein
Ligases
VHL protein, human
Oxygen