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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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A role for MAP kinase in regulating ectodomain shedding of APLP2 in corneal epithelial cells.

We previously reported an increased secretion of amyloid precursor-like protein 2 (APLP2) in the healing corneal epithelium. The present study sought to investigate signal transduction pathways involved in APLP2 shedding in vitro. APLP2 was constitutively shed and released into culture medium in SV40-immortalized human corneal epithelial cells as assessed by Western blotting, flow cytometry, and indirect immunofluorescence. Activation of protein kinase C (PKC) by phorbol 12-myristate 13-acetate (PMA) caused significant increases in APLP2 shedding. This was inhibited by staurosporine and a PKC-epsilon-specific, N-myristoylated peptide inhibitor. Epidermal growth factor (EGF) also induced APLP2 accumulation in culture medium. Basal APLP2 shedding as well as that induced by PMA and EGF was blocked by a mitogen-activated protein kinase (MAPK) kinase inhibitor, U-0126. Our results suggest that MAPK activity accounts for basal as well as PKC- and EGF- induced APLP2 shedding. In addition, PKC-epsilon may be involved in the induction of APLP2 shedding in corneal epithelial cells.[1]

References

  1. A role for MAP kinase in regulating ectodomain shedding of APLP2 in corneal epithelial cells. Xu, K.P., Zoukhri, D., Zieske, J.D., Dartt, D.A., Sergheraert, C., Loing, E., Yu, F.S. Am. J. Physiol., Cell Physiol. (2001) [Pubmed]
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