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PRKCA — RAC1

Pathways - manually collected, often from reviews:

• NCI Pathway Database Syndecan-4-mediated signaling events: RAC1/GDP complex (RAC1) → PKC alpha (PRKCA) (modification, collaborate) Woods et al., Arch Biochem Biophys 2000, Tumova et al., J Biol Chem 2000, Mahalingam et al., J Biol Chem 2007, Bass et al., J Cell Biol 2007
  Evidence: mutant phenotype, assay

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

• IRef Hprd Interaction: PRKCA — RAC1 (in vivo) Slater et al., Biochemistry 2001*
• IRef Intact Interaction: RAC1 — PRKCA (colocalization, imaging technique) Wang et al., EMBO J 2006*
• IRef Ophid Interaction: RAC1 — PRKCA (aggregation, confirmational text mining) Slater et al., Biochemistry 2001*
• IRef Ophid Interaction: RAC1 — PRKCA (aggregation, interologs mapping) Brown et al., Bioinformatics 2005

Text-mined interactions from Literome

Slater et al., Biochemistry 2001 : It was found that the activity of PKCalpha was potently enhanced by RhoA and Cdc42 and to a lesser extent by Rac1 , whereas the effects on the activities of PKCbetaI, -betaII, -gamma, -delta, -epsilon, and -zeta were much reduced
Bass et al., J Cell Biol 2007 : In wild-type fibroblasts, syndecan-4 mediates the matrix induced protein kinase Calpha (PKCalpha) dependent activation of Rac1 and localizes Rac1 activity and membrane protrusion to the leading edge of the cell, resulting in persistent migration
Kim et al., Mol Immunol 2008 (Dermatitis, Allergic Contact...) : PKCalpha and -delta were responsible for increased Rac1 activity and expression of p47(phox), p67(phox)
Kim et al., J Biol Chem 2008 : Protein kinase C (PKC)-alpha and PKCdelta were responsible for increased Rac1 activity, production of ROS, and mediated HA-promoted cell motility
Putnam et al., Cell communication and signaling : CCS 2009 : Loss of PKCalpha expression, but not PKCdelta, by siRNA inhibited Rac and PAK activity as well as invasiveness