Open AccessProtein Kinase C-Delta (PKCδ) Tyrosine Phosphorylation is a Critical Regulator of Neutrophil-Endothelial Cell Interaction in Inflammation
Author(s) -
Fariborz Soroush,
Yuan Tang,
Kimberly Guglielmo,
Alex Engelmann,
Elisabetta Liverani,
Akruti Patel,
Jordan C. Langston,
Shuang Sun,
Satya P. Kunapuli,
Mohammad F. Kiani,
Laurie E. Kilpatrick
Publication year - 2019
Publication title -
shock
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.095
H-Index - 117
eISSN - 1540-0514
pISSN - 1073-2322
DOI - 10.1097/shk.0000000000001247
Subject(s) - protein kinase c , tyrosine phosphorylation , phosphorylation , proinflammatory cytokine , microbiology and biotechnology , tyrosine kinase , inflammation , signal transduction , cancer research , chemistry , biology , endocrinology , immunology
Neutrophil dysfunction plays an important role in inflammation-induced tissue injury. Previously, we identified protein kinase C-δ (PKCδ) as a critical controller of neutrophil activation and trafficking but how PKCδ is regulated in inflammation has not been delineated. PKCδ activity is regulated by tyrosine phosphorylation on multiple sites. Tyrosine155 is a key regulator of apoptosis and gene expression, but its role in proinflammatory signaling is not known.