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Requirements for pseudosubstrate arginine residues during auto-inhibition and phosphatidylinositol-3, 4, 5-(PO4) 3-dependent activation of atypical PKC.

J Biol Chem.. 2014-07; 
Ivey RA, Sajan MP, Farese RV. James A Haley Veterans Medical Center, United States.
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摘要

Atypical protein kinase C (aPKC) isoforms are activated by the phosphatidylinositol 3-kinase product, phosphatidylinositol-3,4,5-(PO4)3 (PIP3). How PIP3 activates aPKC is unknown. Whereas Akt activation involves PIP3 binding to basic residues in the Akt pleckstrin homology domain, aPKCs lack this domain. Here, we examined the role of basic arginine residues common to aPKC pseudosubstrate sequences. Replacement of all five (or certain) arginine residues in the pseudosubstrate sequence of PKC-iota by site-directed mutagenesis led to constitutive activation and unresponsiveness to PIP3 invitro or insulin invivo. However, with addition of exogenous arginine-containing pseudosubstrate tridecapeptide to inhibit this ... More

关键词

diabetes; insulin resistance; phosphatidylinositol kinase (PI Kinase); protein kinase C (PKC); signal transduction
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