Publication: pPKCδ activates SC35 splicing
factor during H9c2 myoblastic differentiation
Authors
Zara, Susi ; Falconi, Mirella ; Rapino, Monica ; Zago, Michela ; Orsini, Giovanna ; Mazzotti, Giovanni ; Cataldi, Amelia ; Teti, Gabriella
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Publisher
Murcia: F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Although Protein Kinase C (PKC) isoforms’
role in the neonatal and adult cardiac tissue development
and ageing has been widely described “in vivo”, the
interaction of such enzymes with specific nuclear
substrates needs to be investigated.
The aim of our research has been the study of the
expression, localization and interaction with the splicing
factor SC35 of PKC isoforms (α, δ, ε, ζ) and their
potential role in modulating the transcription machinery.
H9c2 cells induced to myoblast differentiation in the
presence of 1% Horse Serum (HS) have represented our
experimental model. The expression of PKC isoforms,
their distribution and interaction with SC35 have been
evaluated by western blotting, co-immunoprecipitation
and double gold immunolabeling for transmission and
scanning electron microscopy.
Our results show PKCδ as the most expressed
isoform in differentiated cells. Surprisingly, the
distribution of PKCδ and SC35 does not show any
significant modification between 10%FBS and 1%HS
treated samples and no co-localization is observed.
Moreover the interaction between the phosphorylated
form of PKCδ (pPKCδ) and SC35 increases, is
distributed and co-localizes within the nucleus of
differentiated H9c2.
These data represent reasonable evidence of pPKCδ
mediated SC35 splicing factor activation, suggesting its
direct effect on transcription via interaction with the
transcription machinery. Furthermore, this colocalization
represents a crucial event resulting in downstream changes in transcription of components
which determine the morphological modifications
related to cardiomyoblast differentiated phenotype.
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