NDLI: C-terminal truncation of the retinoblastoma gene product leads to functional inactivation.

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C-terminal truncation of the retinoblastoma gene product leads to functional inactivation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Chen, P. L. Shew, J. Y. Tseng, B. Y. Yang-feng, T. L. Lin, B. T. Lee, W. H.
Description	Author Affiliation: Shew JY ( Department of Pathology, University of California at San Diego, La Jolla 92093.);
Abstract	Mutational inactivation of the retinoblastoma (RB) gene has been implicated in the genesis of retinoblastoma, osteosarcoma, and other human tumors. Our strategy has been to characterize naturally occurring mutants from tumor cells to pinpoint potential domains of RB protein crucial for tumor suppression. We show here that osteosarcoma cell line Saos-2 contains an abnormal endogenous RB protein of 95 kDa (p95) that is located mainly in the cytoplasm. This protein was identified by antibodies recognizing several different RB epitopes, but not by one directed solely against the C terminus, suggesting C-terminal truncation. This conclusion was supported by analysis of mRNA and genomic DNA, which revealed that a transcriptionally active RB allele had a deletion of exons 21-27. In contrast to normal RB protein, this truncated protein was not phosphorylated and did not bind to the large tumor (T) antigen encoded by simian virus 40. We previously reported that introduction of normal RB protein into Saos-2 cells suppressed their neoplastic phenotype, indicating functional inactivation of their endogenous RB genes. These results provide an initial step to elucidate domains crucial to the cancer-suppression function of RB protein; its C-terminal portion is evidently important for this activity.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	1
Volume Number	87
Language	English
Publisher	National Academy of Sciences
Publisher Date	1990-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Eye Neoplasms Genetics Genes Mutation Retinoblastoma Protein Retinoblastoma Suppression, Genetic Animals Antibodies Cell Line Chromosome Deletion DNA Probes Immunoblotting Molecular Sequence Data Neoplasm Proteins Polymerase Chain Reaction RNA-Directed DNA Polymerase Restriction Mapping Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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