Characterization of the gene ( VBP1) and transcript for the von Hippel-Lindau binding protein and isolation of the highly conserved murine homologue.
A single-copy, widely expressed gene of at least 30 kb and six exons was discovered via a hybrid mRNA resulting from an inversion causing hemophilia A. A segment of the 1.7-kb message of this gene has been shown by others to encode a protein (named VBP1) interacting with the product of the von Hippel-Lindau gene and thus is expected to participate in pathways involving this tumor suppressor gene. The mouse VBP1 message we isolated encodes a polypeptide of 160 residues absolutely identical to that of human. Even the 3' untranslated tails of the mRNAs show 68% conservation, and both use the unusual ATTAAA polyadenylation signal. The mouse gene has a single transcription start while the human homologue has two major starts and a minor start. This could result in amino-end extensions of the human protein. A polymorphism with 42% heterozygosity in the United Kingdom population was detected in the 3' tail of the message. VBP1 is unlike other known proteins but a consensus for tyrosine phosphorylation possibly suggests regulation by kinases.[1]References
- Characterization of the gene (VBP1) and transcript for the von Hippel-Lindau binding protein and isolation of the highly conserved murine homologue. Brinke, A., Green, P.M., Giannelli, F. Genomics (1997) [Pubmed]
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