scholarly journals Possible role of atypical protein kinase C activated by arachidonic acid in Ca2+ sensitization of rabbit smooth muscle.

1997 ◽  
Vol 500 (1) ◽  
pp. 95-109 ◽  
Author(s):  
P Gailly ◽  
M C Gong ◽  
A V Somlyo ◽  
A P Somlyo
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Atypical Protein Kinase C ◽  
Atypical Protein Kinase ◽  
Kinase C

Role of atypical protein kinase C isozymes and NF-κB in IL-1β-induced expression of cyclooxygenase-2 in human myometrial smooth muscle cells

2006 ◽  
Vol 210 (3) ◽  
pp. 637-643 ◽  
Author(s):  
Sara V. Duggan ◽  
Tamsin Lindstrom ◽  
Teresa Iglesias ◽  
Phillip R. Bennett ◽  
Giovanni E. Mann ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Atypical Protein Kinase C ◽  
Induced Expression ◽  
Atypical Protein Kinase ◽  
Kinase C

scholarly journals The critical role of atypical protein kinase C in activating hepatic SREBP-1c and NFκB in obesity

2009 ◽  
Vol 50 (6) ◽  
pp. 1133-1145 ◽  
Author(s):  
Mini P. Sajan ◽  
Mary L. Standaert ◽  
Sonali Nimal ◽  
Usha Varanasi ◽  
Tina Pastoor ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Critical Role ◽  
Atypical Protein Kinase C ◽  
Atypical Protein Kinase ◽  
Kinase C

scholarly journals The Drosophila Atypical Protein Kinase C-Ref(2)P Complex Constitutes a Conserved Module for Signaling in the Toll Pathway

2002 ◽  
Vol 22 (24) ◽  
pp. 8787-8795 ◽  
Author(s):  
Antonia Avila ◽  
Neal Silverman ◽  
María T. Diaz-Meco ◽  
Jorge Moscat
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Nuclear Translocation ◽  
Critical Role ◽  
Atypical Protein Kinase C ◽  
Atypical Protein Kinase ◽  
Kinase C ◽  
P Protein ◽  
Toll Signaling

ABSTRACT Recent results showed the critical role of the mammalian p62-atypical protein kinase C (aPKC) complex in the activation of NF-κB in response to different stimuli. Here we demonstrate using the RNA interference technique on Schneider cells that the Drosophila aPKC (DaPKC) is required for the stimulation of the Toll-signaling pathway, which activates the NF-κB homologues Dif and Dorsal. However, DaPKC does not appear to be important for the other Drosophila NF-κB signaling cascade, which activates the NF-κB homologue Relish in response to lipopolysaccharides. Interestingly, DaPKC functions downstream of the nuclear translocation of Dorsal or Dif, controlling the transcriptional activity of the Drosomycin promoter. We also show that the Drosophila Ref(2)P protein is the homologue of mammalian p62 as it binds to DaPKC, its overexpression is sufficient to activate the Drosomycin but not the Attacin promoter, and its depletion severely impairs Toll signaling. Collectively, these results demonstrate the conservation of the p62-aPKC complex for the control of innate immunity signal transduction in Drosophila melanogaster.

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