PLCâ1a and PLCâ1b selective regulation and cyclin D3 modulation reduced by Kinamycin F during K562 cell differentiation. (Articolo in rivista)

Type
Label
  • PLCâ1a and PLCâ1b selective regulation and cyclin D3 modulation reduced by Kinamycin F during K562 cell differentiation. (Articolo in rivista) (literal)
Anno
  • 2014-01-01T00:00:00+01:00 (literal)
Alternative label
  • Bavelloni A, Dmitrienko GI, Goodfellow VJ, Ghavami A, Piazzi M, Blalock W, Chiarini F, Cocco L, Faenza I. (2014)
    PLCâ1a and PLCâ1b selective regulation and cyclin D3 modulation reduced by Kinamycin F during K562 cell differentiation.
    in Journal of cellular physiology (Print)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Bavelloni A, Dmitrienko GI, Goodfellow VJ, Ghavami A, Piazzi M, Blalock W, Chiarini F, Cocco L, Faenza I. (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Laboratory of Musculoskeletal Cell Biology, Rizzoli Orthopedic Institute, Bologna, Italy; Laboratory RAMSES, Rizzoli Orthopedic Institute, Bologna, Italy; Department of Chemistry, University of Waterloo, Waterloo, Ontario, Canada; School of Pharmacy, University of Waterloo, Waterloo, Ontario, Canada; Cell Signaling Laboratory, Department of Biomedical Sciences, University of Bologna, Bologna, Italy; CNR-National Research Council of Italy, Institute of Molecular Genetics, Bologna, Italy. (literal)
Titolo
  • PLCâ1a and PLCâ1b selective regulation and cyclin D3 modulation reduced by Kinamycin F during K562 cell differentiation. (literal)
Abstract
  • Here we report that both PLCâ1a and PLCâ1b are relevant regulators of erythropoiesis in that kinamycin F, a potent inducer of ?-globin production in K562 cells, caused a selectively reduction of both PLCâ1 isozymes even though the results point out that the effect of the drug is mainly directed toward the expression of the PLCâ1a isoform. We have identified a different role for the two isozymes as regulators of K562 differentiation process induced by kinamycin F. The overexpression of PLCâ1b induced an increase in ?-globin expression even in the absence of kinamycin F. Moreover during K562 differentiation, cyclin D3 level is regulated by PLCâ1 signaling pathway. Namely the amplification of the expression of the PLCâ1a, but not of PLCâ1b, 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 PLCâ1b is mainly present in the nucleus in respect to PLCâ1a. Our data indicate that the amplification of PLCâ1a expression, following treatment with kinamycin F, confers a real advantage to K562 cells viability and protects cells themselves from apoptosis. J. Cell. Physiol. © 2014 Wiley Periodicals, Inc. (literal)
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