PuSH - Publikationsserver des Helmholtz Zentrums München

Mischak, H. ; Pierce, J.H.* ; Goodnight, J.* ; Kazanietz, M.G.* ; Blumberg, P.M.* ; Mushinski, J.F.*

Phorbol ester-induced myeloid differentiation is mediated by protein kinase C-α and -δ and not by protein kinase C-βII, -ε, -ζ, and -η.

J. Biol. Chem. 268, 20110-20115 (1993)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
It is generally accepted that the multiple, similar protein kinase C (PKC) isozymes are responsible for different specialized physiological processes, but evidence that directly assigns specific functions to specific isozymes is scarce. To test whether specific PKC isozymes are involved in myeloid differentiation, we have studied the effect of overexpression of PKC-α, -βII, -δ, -ε, -ζ and -η in 32D, a mouse myeloid progenitor cell line that does not differentiate in response to 12-O-tetradecanoylphorbol-13-acetate (TPA). No significant morphological or phenotypic changes could be observed in unstimulated cells that overexpress any of these isozymes. However, the cell lines that overexpressed PKC-α or -δ had acquired the ability to become mature macrophages 2-6 h after TPA stimulation. The overexpression of PKC-βII, -ε, -ζ, or -η, in contrast, did not permit TPA-induced differentiation. These results indicate that only these two members of the PKC gene family can participate in TPA-induced myeloid differentiation.
Altmetric
Weitere Metriken?
[➜Einloggen]
Zusatzinfos bearbeiten [➜Einloggen]
Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
ISSN (print) / ISBN 0021-9258
e-ISSN 1083-351X
Zeitschrift Journal of Biological Chemistry, The
Quellenangaben Band: 268, Heft: 27, Seiten: 20110-20115 Artikelnummer: , Supplement: ,
Verlag American Society for Biochemistry and Molecular Biology
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Clinical Molecular Biology and Tumor Genetics (K.MOLBI)