S-Space College of Medicine/School of Medicine (의과대학/대학원) Dept. of Biochemistry & Molecular Biology (생화학교실) Journal Papers (저널논문_생화학교실)
Hematopoietic malignancies associated with increased Stat5 and Bcl-x(L) expressions in Ink4a/Arf-deficient mice
- Issue Date
- Mech Ageing Dev. 2005 Jun-Jul;126(6-7):732-9.
- Animals ; Cyclin-Dependent Kinase Inhibitor p16/*deficiency ; DNA-Binding Proteins/*biosynthesis ; Gene Expression Regulation, Neoplastic/genetics ; Hematologic Neoplasms/genetics/*metabolism ; Mice ; Mice, Knockout ; Milk Proteins/*biosynthesis ; Proto-Oncogene Proteins c-bcl-2/*biosynthesis ; STAT5 Transcription Factor ; Signal Transduction/genetics ; Trans-Activators/*biosynthesis ; Tumor Suppressor Protein p14ARF/*deficiency ; bcl-X Protein ; Hematopoiesis
- The INK4a/ARF locus, which encodes the two distinct proteins p16(INK4a) and p14(ARF), is frequently altered in various hematological malignancies as well as in other types of cancers in humans. In this study, we surveyed tumors that had spontaneously developed in Ink4a/Arf-deficient mice with an inbred FVB/NJ genetic background. We found that an Ink4a/Arf-deficiency exerted more severe effects on the induction of hematopoietic malignancies in mice with an inbred FVB/NJ genetic background than in mice with a mixed genetic background. We also provided the evidence that this prevalence of hematopoietic malignancies in Ink4a/Arf-deficient mice is associated with the upregulated expressions of Stat5 and its transcriptional target, Bcl-x(L), both of which are involved in the regulation of hematopoiesis. These results suggest a possible implication of the Ink4a/Arf locus in the control of hematopoietic pathways by negatively regulating the Stat5-signalling pathways.
- 0047-6374 (Print)
- Files in This Item: There are no files associated with this item.