Interferon beta increases c-Myc proteolysis in mouse monocyte/macrophage leukemia cells.
Leuk Res
; 29(11): 1307-14, 2005 Nov.
Article
en En
| MEDLINE
| ID: mdl-15939469
ABSTRACT
Growth inhibitory activity of interferons (IFNs) has been attributed to several events. These include rapid induction of cyclin-dependent kinase inhibitors, such as those in the Cip/Kip and Ink 4 families and down-regulation of c-myc mRNA and c-Myc transcriptional activity. Here, we report an additional mechanism, involving regulation of Myc protein levels, through which type 1 IFN may halt proliferation of cells. This was discovered using a cell line which constitutively expresses c-myc from a retrovirus vector and which was reported to have undergone deletion of genes encoding the Ink 4 tumor suppressors p15 and p16. IFNbeta caused a reduction in the steady state level of c-Myc protein by increasing degradation through the 26S proteasome. Our data, as well as that of others, indicate that multiple levels of c-Myc expression can be affected by IFN treatment and this contributes to rapid growth arrest in the G1 phase of the cell cycle.
Buscar en Google
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Proteínas Proto-Oncogénicas c-myc
/
Interferón beta
Límite:
Animals
Idioma:
En
Revista:
Leuk Res
Año:
2005
Tipo del documento:
Article
País de afiliación:
Estados Unidos