Skip interacts with the retinoblastoma tumor suppressor and inhibits its transcriptional repression activity
AUTOR(ES)
Prathapam, Tulasiram
FONTE
Oxford University Press
RESUMO
Ski interacting protein (Skip) plays an important role in the transforming activity of both v-Ski and EBNA2 (Epstein–Barr virus encoded latency protein) and is involved in EBNA2 and NotchIC activation of CBF1-repressed promoters. We have previously shown that Skip acts as a transcriptional co-activator on a number of cellular and viral promoters. Here, we report that Skip also interacts with pRb and, in cooperation with Ski, can overcome pRb-induced transcriptional repression. We show a strong and direct interaction between pRb and Skip, and we map the site of interaction to amino acid residues 171–353 of the evolutionarily conserved SNW domain of Skip. Furthermore, the combination of Skip and Ski can successfully overcome the G1 arrest and flat cell phenotype induced by pRb. Taken together, these studies suggest that one potential function of the Skip–Ski complex is to overcome the growth-suppressive activities of pRb.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=137971Documentos Relacionados
- The retinoblastoma gene product interacts with maintenance human DNA (cytosine-5) methyltransferase and modulates its activity
- Sp100 Interacts with ETS-1 and Stimulates Its Transcriptional Activity
- Distinct Mechanisms for Repression of RNA Polymerase III Transcription by the Retinoblastoma Tumor Suppressor Protein
- Tissue-specific tumor suppressor activity of retinoblastoma gene homologs p107 and p130
- Clefts, grooves, and (small) pockets: The structure of the retinoblastoma tumor suppressor in complex with its cellular target E2F unveiled