Article

The protein kinase C (PKC) family of proteins in cytokine signaling in hematopoiesis.

Robert H. Lurie Comprehensive Cancer Center and Division of Hematology-Oncology, Northwestern University Medical School, 300 East Superior Street, Chicago, IL 60611, USA.
Journal of Interferon & Cytokine Research (impact factor: 3.06). 09/2007; 27(8):623-36. DOI:10.1089/jir.2007.0007 pp.623-36
Source: PubMed

ABSTRACT The members of the protein kinase C (PKC) family of proteins play important roles in signaling for various growth factors, cytokines, and hormones. Extensive work over the years has led to the identification of three major groups of PKC isoforms. These include the classic PKCs (PKCalpha, PKCbeta(I), PKCbeta(II), PKCgamma), the novel PKCs (PKCdelta, PKCepsilon, PKCeta, PKCmu, PKCtheta), and the atypical PKCs (PKCzeta, PKCiota/lambda). All these PKC subtypes have been shown to participate in the generation of signals for important cellular processes and to mediate diverse and, in some cases, opposing biologic responses. There is emerging evidence that these kinases also play key functional roles in the regulation of cell growth, apoptosis, and differentiation of hematopoietic cells. In this review, both the engagement of the various PKC members in cytokine and growth factor signaling and their role in the regulation of hematopoiesis are discussed.

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    Article: Role for PKC δ in Fenretinide-Mediated Apoptosis in Lymphoid Leukemia Cells.
    Vivian R Ruvolo, Kul B Karanjeet, Todd F Schuster, Rhoderick Brown, Yibin Deng, Edward Hinchcliffe, Peter P Ruvolo
    [show abstract] [hide abstract]
    ABSTRACT: The synthetic Vitamin A analog fenretinide is a promising chemotherapeutic agent. In the current paper, the role of PKC δ was examined in fenretinide-induced apoptosis in lymphoid leukemia cells. Levels of proapoptotic cleaved PKC δ positively correlated with drug sensitivity. Fenretinide promoted reactive oxygen species (ROS) generation. The antioxidant Vitamin C prevented fenretinide-induced PKC δ cleavage and protected cells from fenretinide. Suppression of PKC δ expression by shRNA sensitized cells to fenretinide-induced apoptosis possibly by a mechanism involving ROS production. A previous study demonstrated that fenretinide promotes degradation of antiapoptotic MCL-1 in ALL cells via JNK. Now we have found that fenretinide-induced MCL-1 degradation may involve PKC δ as cleavage of the kinase correlated with loss of MCL-1 even in cells when JNK was not activated. These results suggest that PKC δ may play a complex role in fenretinide-induced apoptosis and may be targeted in antileukemia strategies that utilize fenretinide.
    Journal of signal transduction. 01/2010; 2010:584657.
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Keywords

atypical PKCs
 
biologic responses
 
cell growth
 
cellular processes
 
classic PKCs
 
cytokines
 
diverse
 
growth factor signaling
 
hematopoiesis
 
hematopoietic cells
 
key functional roles
 
kinases
 
novel PKCs
 
PKC isoforms
 
PKCiota/lambda
 
PKCtheta
 
protein kinase C
 
signals
 
various growth factors
 
various PKC members
 

Amanda J Redig