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

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 NH...

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Bibliographic Details
Published in:Leukemia research 2006-02, Vol.30 (2), p.153-163
Main Authors: Qi, Chen-Feng, Xiang, Shao, Shin, Min Sun, Hao, Xingpei, Lee, Chang Hoon, Zhou, Jeff X., Torrey, Ted A., Hartley, Janet W., Fredrickson, Torgny N., Morse, Herbert C.
Format: Article
Language:English
Subjects:
Animals
Cell Line, Tumor
Cell-cycle regulation
Cyclin D1 - analysis
Cyclin D3
Cyclin E - analysis
Cyclin-Dependent Kinase Inhibitor p27 - analysis
Cyclin-Dependent Kinase Inhibitor p27 - genetics
Cyclin-Dependent Kinase Inhibitor p27 - metabolism
Cyclins - analysis
Immunohistochemistry
Ki-67 Antigen - analysis
Lymphoma, B-Cell - chemistry
Mice
Mice, Inbred C57BL
Mouse B cell lymphoma
p27
Phosphorylation
Proto-Oncogene Proteins c-akt - analysis
RNA, Messenger - analysis
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Summary: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.
ISSN:0145-2126
1873-5835
DOI:10.1016/j.leukres.2005.06.025