PKCdelta splicing variant (PKCdeltaIII) induces neurite outgrowth in PC12 cells in the absence of NGF
Hiroyuki Yamasaki, Tomoko NakaiiD, Kanae Kitatani, Chikara Kato, Susumu TakekoshiiD
Abstract
Protein kinase C (PKC){delta} is a serine/threonine kinase involved in many cellular processes in response to diverse stimuli, including cell proliferation, differentiation, apoptosis, tumor inhibition, and cell migration. PKC{delta} consists of the N terminal regulatory domain and the C terminal catalytic domain, which are linked with a hinge region. An alternative splicing variant of rat PKC{delta} (also known as PKC{delta}III) has been reported, and this PKC{delta} splicing variant (SV) has only the regulatory domain without the catalytic domain. However, its function remains unclear. In this study, we found that PKC{delta} SV induced neurite outgrowth in the absence of nerve growth factor (NGF) in PC12 cells. Immunoblot analysis revealed that ERK was phosphorylated by NGF treatment, but not by PKC{delta} SV induction, indicating that PKC{delta} SV-mediated neurite outgrowth was different from NGF-mediated one. In addition, we showed that PKC{delta} full length and SV increased their mRNA expression after NGF treatment and that PKC{delta} SV was more susceptible to its proteasomal degradation. Our findings provided insights into the role of PKC{delta} SV in neurite outgrowth.
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