The INK4a/ARF locus in murine tumorigenesis.
The INK4a/ARF locus is regarded as one of the most important anti-tumoral defenses that mammalian organisms possess. The characterization of its two gene products, p16(INK4a) and p19(ARF), has provided a great insight on the functioning of the tumor suppressors Rb and p53, respectively. Present evidence indicates that the INK4a/ARF locus is transcriptionally activated by oncogenic stresses, resulting in cell-cycle arrest or apoptosis. Here, I review the evidence accumulated on the involvement of the INK4a/ARF locus in murine tumorigenesis. Also, I summarize the phenotype of the different transgenic mouse models based on the inactivation of the INK4a/ARF locus.
Serrano
M
M
Department of Immunology and Oncology, Centro Nacional de Biotecnología, Campus de Cantoblanco, Madrid E-28049, Spain. mserrano@cnb.uam.es.
D000483:Alleles; D000818:Animals; D002352:Carrier Proteins / Q000235:genetics*; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D019941:Cyclin-Dependent Kinase Inhibitor p16; D016147:Genes, Tumor Suppressor; D020022:Genetic Predisposition to Disease; D051379:Mice; D008822:Mice, Transgenic
D002352:Carrier Proteins; D019941:Cyclin-Dependent Kinase Inhibitor p16