Phospholipase C (PLC) has been known to be a key effector protein in signal transduction pathway
for cell proliferation and differentiation.
Studies on signalling through the insulin/IGF-1 receptors in muscle differentiation have revealed
that PLCγ1 is involved during this process and that both mRNA and protein levels were increased
during myogenesis. Based on increasing signal transduction pathways that required both PLCγ1 and
PKCε, we investigated its role in insulin stimulation of skeletal muscle differentiation. The precise
effects of insulin on specific PKC isoforms are as yet unknown. Insulin stimulation produced a
gradual increase in PKCε expression and activation of PKCε through skeletal muscle
differentiation. By immunoprecipitation we have demonstrated that endogenous PLCγ1 and PKCε
belong to the same immunocomplex that increase during through myogenic differentiation.
Furthermore, the SH domain of PLCγ1 is involved in the protein complex and that its confine to the
Golgi membrane. PLCγ1 has been involved in cyclin D3 up-regulation. By overexpression and
silencing approach we have evidenced that PKCε modulate the espression of cyclin D3; the kinase
dead form of PKCε doesn’t maintain the same ability. Using a reporter hGH vector we proved that
PKCε acts at transcriptional level by affecting the -37 region of cyclin D3 promoter, as has been
described previous for PLCγ1. In summary this data proved the involvement of PKCε in the
regulation of cyclin D3 expression, together with PLCγ1.
| Identifer | oai:union.ndltd.org:unibo.it/oai:amsdottorato.cib.unibo.it:1076 |
| Date | 26 May 2008 |
| Creators | Gaboardi, Gian Carlo <1978> |
| Contributors | Cocco, Lucio Ildebrando |
| Publisher | Alma Mater Studiorum - Università di Bologna |
| Source Sets | Università di Bologna |
| Language | Italian |
| Detected Language | English |
| Type | Doctoral Thesis, PeerReviewed |
| Format | application/pdf |
| Rights | info:eu-repo/semantics/openAccess |
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