Increased p27Kip1 Cyclin-Dependent Kinase Inhibitor Gene Expression Following Anti-IgM Treatment Promotes Apoptosis of WEHI 231 B Cells
| Autor: | M, Wu, R E, Bellas, J, Shen, W, Yang, G E, Sonenshein |
|---|---|
| Rok vydání: | 1999 |
| Předmět: |
Cyclin-Dependent Kinase Inhibitor p21
CD40 Ligand Immunology Apoptosis Cell Cycle Proteins Ligands Proto-Oncogene Proteins c-myc Mice Cyclins Tumor Cells Cultured Animals Immunology and Allergy RNA Antisense CD40 Antigens Enzyme Inhibitors B-Lymphocytes Membrane Glycoproteins Tumor Suppressor Proteins Oligonucleotides Antisense Cyclin-Dependent Kinases Antibodies Anti-Idiotypic Gene Expression Regulation Neoplastic Immunoglobulin M Tumor Suppressor Protein p53 Microtubule-Associated Proteins Cyclin-Dependent Kinase Inhibitor p27 Signal Transduction |
| Zdroj: | The Journal of Immunology. 163:6530-6535 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.163.12.6530 |
| Popis: | Engagement of the B cell receptor of WEHI 231 immature B cells leads sequentially to a drop in c-Myc, to induction of the cyclin-dependent kinase inhibitor p27Kip1, and finally to apoptosis. Recently we demonstrated that the drop in c-Myc expression promotes cell death, whereas the induction of p27 has been shown to lead to growth arrest. In this paper, we demonstrate that increased p27 expression also promotes apoptosis of WEHI 231 B cells. The rescue of WEHI 231 cells by CD40 ligand engagement of its receptor prevented the increase in p27 induction. Inhibition of p27-ablated apoptosis induced upon expression of antisense c-myc RNA. Furthermore, specific induction of p27 gene expression resulted in apoptosis of WEHI 231 cells. Lastly, inhibition of expression of c-Myc, upon induction of an antisense c-myc RNA vector, was sufficient to induce increased p27 levels and apoptosis. Thus, these findings define a signaling pathway during B cell receptor engagement in which the drop in c-Myc levels leads to an increase in p27 levels that promotes apoptosis. |
| Databáze: | OpenAIRE |
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