KT5823 activates human neutrophils and fails to inhibit cGMP-dependent protein kinase phosphorylation of vimentin.
The effectiveness of the cGMP-dependent protein kinase inhibitor, KT5823, was investigated in human neutrophils. KT5823 did not inhibit the cGMP-dependent protein kinase mediated in vitro, or in situ phosphorylation of vimentin, a known substrate for this enzyme in activated neutrophils. In addition, KT5823 was shown to induce dramatic shape changes in neutrophils, suggesting it has an activating effect upon the cells.
Wyatt
T A
TA
Department of Pathology, University of North Carolina, Chapel Hill 27599-7525.
Pryzwansky
K B
KB
Lincoln
T M
TM
D000470:Alkaloids / Q000494:pharmacology*; D002227:Carbazoles; D006152:Cyclic GMP / Q000378:metabolism*; D004586:Electrophoresis; D005455:Fluorescent Antibody Technique; D006657:Histones / Q000378:metabolism; D006801:Humans; D007211:Indoles; D009504:Neutrophils / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D009842:Oligopeptides / Q000378:metabolism; D010766:Phosphorylation; D047428:Protein Kinase Inhibitors; D011494:Protein Kinases / Q000378:metabolism*; D014746:Vimentin / Q000378:metabolism*
D000470:Alkaloids; D002227:Carbazoles; D006657:Histones; D007211:Indoles; D009842:Oligopeptides; D047428:Protein Kinase Inhibitors; D014746:Vimentin; C073601:KT 5823; C037642:kemptide; D011494:Protein Kinases; D006152:Cyclic GMP