Tumor Suppression by a Severely Truncated Species of Retinoblastoma Protein
AUTOR(ES)
Yang, Hong
FONTE
American Society for Microbiology
RESUMO
Rb+/+:Rb−/− chimeric mice are healthy until early in adulthood when they develop lethal pituitary tumors composed solely of Rb−/− cells. In an effort to delineate the minimal structures of the retinoblastoma protein necessary for RB tumor suppression function, chimeric animals derived from stably transfected RB−/− embryonic stem (ES) cells were generated. One such ES cell transfectant expressed a human RB allele encoding a stable, truncated nuclear derivative lacking residues 1 to 378 (Δ1-378). Others encoded either wild-type human RB or an internally deleted derivative of the Δ1-378 mutant. All gave rise to viable chimeric animals with comparable degrees of chimerism. However, unlike control mice derived, in part, from naive Rb−/− ES cells or from ES cells transformed by the double RB mutant, Δ1-378/Δexon22, animals derived from either wild-type RB- or Δ1-378 RB-producing ES cells failed to develop pituitary tumors. Thus, in this setting, a substantial fraction of the RB sequence is unnecessary for RB-mediated tumor suppression.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=133747Documentos Relacionados
- Enhanced tumor cell growth suppression by an N-terminal truncated retinoblastoma protein.
- Mutations of N-terminal regions render the retinoblastoma protein insufficient for functions in development and tumor suppression.
- Growth suppression by p16ink4 requires functional retinoblastoma protein.
- Regulation of Cellular Genes in a Chromosomal Context by the Retinoblastoma Tumor Suppressor Protein
- The block of adipocyte differentiation by a C-terminally truncated, but not by full-length, simian virus 40 large tumor antigen is dependent on an intact retinoblastoma susceptibility protein family binding domain.
