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PLC_1a and PLC_1b selective regulation and cyclin D3 modulation reduced by kinamycin F during k562 cell differentiation.

Autori

Bavelloni A, Dmitrienko GI, Goodfellow VJ, Ghavami A, Piazzi M, Blalock W, Chiarini F, Cocco L, Faenza I.

Riferimenti

JOURNAL OF CELLULAR PHYSIOLOGY 230(3) 587-594, 2015

Autori CNR

BLALOCK, CHIARINI

Moduli

Abstract

Here we report that both PLC_1a and PLC_1b are relevant regulators of erythropoiesis in that kinamycin F, a potent inducer of _-globin production in K562 cells, caused a selectively reduction of both PLC_1 isozymes even though the results point out that the effect of the drug is mainly directed toward the expression of the PLC_1a isoform. We have identified a different role for the two isozymes as regulators of K562 differentiation process induced by kinamycin F. The overexpression of PLC_1b induced an increase in _-globin expression even in the absence of kinamycin F. Moreover during K562 differentiation, cyclin D3 level is regulated by PLC_1 signaling pathway. Namely the amplification of the expression of the PLC_1a, but not of PLC_1b, is able to maintain high levels of expression of cyclin D3 even after treatment with kinamycin F. This could be due to their different distribution in the cell compartments since the amount of PLC_1b is mainly present in the nucleus in respect to PLC_1a. Our data indicate that the amplification of PLC_1a expression, following treatment with kinamycin F, confers a real advantage to K562 cells viability and protects cells themselves from apoptosis. 2014 Wiley Periodicals, Inc., A Wiley Company.

Link all articolo

http://onlinelibrary.wiley.com/doi/10.1002/jcp.24776/abstract

Parole Chiave

Note

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