Abstract
Protein kinase C (PKC)-θ is a serine/threonine kinase belonging to the calcium-independent novel PKC subfamily; its expression is restricted to certain tissues and cell types, including T cells. The signals delivered from T cell receptor (TCR) and CD28 costimulatory molecules trigger PKC-θ catalytic activation and membrane translocation to the immunological synapse, leading to activation of NF-κB, AP-1, and NF-AT. These transcription factors are important for T cell survival, activation, and differentiation. Phosphorylation of PKC-θ at multiple Ser/Thr/Tyr residues is induced in T cells during TCR signaling. Some phosphorylation sites play critical roles in the regulation of PKC-θ function and downstream signaling. The regulation mechanisms for PKC-θ phosphorylation sites are now being revealed. In this review, we discuss the current understanding of the regulation of PKC-θ function by phosphorylation during TCR signaling.
Highlights
Protein kinase C (PKC)-θ was originally cloned in 1993 as a novel member of the PKC gene family (Baier et al, 1993; Chang et al, 1993)
The unphosphorylated turn motif in PKC-βII is bound to HSP70, which stabilizes PKC-βII, allowing re-phosphorylation of this enzyme (Gao and Newton, 2002); this study suggests that PKC-θ S676A may be more stable and ready for autophosphorylation at T538 due to a loss of phosphorylation in the turn motif of this mutant
Phosphorylations play critical roles in regulating PKC-θ catalytic activity and membrane translocation, both of which are required for the proper function of PKC-θ in T cell activation
Summary
Protein kinase C (PKC)-θ was originally cloned in 1993 as a novel member of the PKC gene family (Baier et al, 1993; Chang et al, 1993). T219 phosphorylation of PKC-θ is undetectable in the kinase-dead PKC-θ K409R mutant in Jurkat T cells upon cellular stimulation, suggesting that T219 is an inducible autophosphorylation site of PKC-θ during T cell activation (Thuille et al, 2005).
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