is Íslenska en English


Háskóli Íslands > Heilbrigðisvísindasvið > Rit starfsmanna >

Vinsamlegast notið þetta auðkenni þegar þið vitnið til verksins eða tengið í það:

  • Titill er á ensku The v-erbA oncoprotein of the AEV transforming retrovirus binds to the promoter region of the erythroid specific band 3 gene
  • 1994
  • Útdráttur er á ensku

    Avian erythroblastosis virus (AEV) which carries two oncogenes, v-erbA and v-erbB causes erythroleukemia and sarcomas in young chickens and transforms embryo fibroblasts and bone marrow cells in culture. The v-erbA oncogene encodes an aberrant version of a gene for a nuclear thyroid hormone receptor (c-erbA, TR) and functions in neoplasia by blocking erythroid differentiation and by altering the growth properties of fibroblasts. Owing to the multiple point mutations and a small C-terminal deletion, v-erbA has lost the ability to bind T3, but still binds to DNA in a sequence-specific fashion. The phenotypic effects of v-erbA are correlated with and probably caused by v-erbA-mediated repression of a set of erythrocyte-specific genes, but their expression seems to be required during normal erythrocyte maturation. In differentiating erythroblasts the v-erbA oncoprotein specifically arrests expression of the avian erythrocyte anion transporter (band 3), CAII and ALA-S genes at the transcriptional level. Overexpression of the TK is required to modulate erythrocyte-specific gene expression in the presence of T3. The v-erbA oncogene might act as a constitutively active repressor of erythrocyte gene transcription, having lost its ability to depress (or activate) these genes in response to T3 or even retinoic acid.

Birtist í: 
  • Annals of the New York Academy of Sciences 1994, 724, 426-429
  • 0077-8923
  • 0-89766-844-8
Tengd vefslóð: 
  • 18.2.2015

Skráarnafn Stærð AðgangurLýsingSkráartegund 
AnnNYAcadSci94.pdf364.89 kBOpinnHeildartextiPDFSkoða/Opna