Expression of the cyclin-dependent kinase inhibitor p27 and its deregulation in mouse B cell lymphomas.

Autor: Qi CF; Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, Twinbrook I, Room 1421, National Institutes of Health, Rockville, MD, USA., Xiang S, Shin MS, Hao X, Lee CH, Zhou JX, Torrey TA, Hartley JW, Fredrickson TN, Morse HC 3rd
Jazyk: angličtina
Zdroj: Leukemia research [Leuk Res] 2006 Feb; Vol. 30 (2), pp. 153-63. Date of Electronic Publication: 2005 Aug 24.
DOI: 10.1016/j.leukres.2005.06.025
Abstrakt: CDKN1B (p27) regulates cell-cycle progression at the G1-S transition by suppressing the cyclin E/CDK2 kinase complex. In normal lymphocytes and most human B cell non-Hodgkin lymphomas (NHL), there is an inverse correlation between proliferative activity and expression of p27; however, a subset of NHL with high mitotic indices expresses p27, which is inactive due to sequestration in nuclear protein complexes or due to cytoplasmic retention. Our studies of mouse B cell NHL also identified cases with high proliferative activity and high levels of p27 at a surprisingly high frequency. Here, p27 was complexed with D-type cyclins 1 and 3 and with the COPS9 protein, JAB1. In addition, we found cytoplasmic sequestration following phosphorylation by activated AKT.
Databáze: MEDLINE