Publication details
Mechanismus suprese onkoproteinu v-myb proteinem jun v buňkách BM2: aktivace receptoru pro kyselinu retinovou
| Title in English | Mechanism of v-Myb-suppression by Jun protein in BM2 cells: activation of retinoic acid receptor |
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| Authors | |
| Year of publication | 2003 |
| Type | Article in Proceedings |
| Conference | Sborník příspěvků, VII. pracovní setkání biochemiků a molekulárních biologů |
| MU Faculty or unit | |
| Citation | |
| Field | Oncology and hematology |
| Keywords | Myb; Jun; differentiation; transactivation |
| Description | BM2 cells constitutively express AMV v-myb. We showed earlier that one way how to reduce high proliferation rate of these leukemic cells and induce their terminal differentiation is to increase intracellular level of Jun proteins. Therefore, we derived BM2 cell line variants inducibly expressing v-jun (BM2vJUN) and c-jun (BM2cJUN) and found several jun-induced changes of BM2 phenotype. One of the features we found in both BM2vJUN and BM2cJUN cells was increased sensitivity to retinoic acid (RA). It was described earlier that RA can induce terminal differentiation of BM2 cells but this effect was strictly dependent on increased level of nuclear retinoic acid receptors RAR or RXR. Interestingly, we found similar effect also in BM2 cells expressing jun, although Jun protein did not affect expression level of endogenous RAR and/or RXR expression. However, transcription activation capability of RAR protein was significantly upregulated in BM2 cells expressing Jun causing suppression of function of transforming v-Myb oncoprotein. |
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