Structural highlights
Disease
[PAK3_HUMAN] X-linked non-syndromic intellectual disability. The disease is caused by mutations affecting the gene represented in this entry.
Function
[PAK3_HUMAN] Serine/threonine protein kinase that plays a role in a variety of different signaling pathways including cytoskeleton regulation, cell migration, or cell cycle regulation. Plays a role in dendrite spine morphogenesis as well as synapse formation and plasticity. Acts as downstream effector of the small GTPases CDC42 and RAC1. Activation by the binding of active CDC42 and RAC1 results in a conformational change and a subsequent autophosphorylation on several serine and/or threonine residues. Phosphorylates MAPK4 and MAPK6 and activates the downstream target MAPKAPK5, a regulator of F-actin polymerization and cell migration. Additionally, phosphorylates TNNI3/troponin I to modulate calcium sensitivity and relaxation kinetics of thin myofilaments. May also be involved in early neuronal development.[1]
References
- ↑ Deleris P, Trost M, Topisirovic I, Tanguay PL, Borden KL, Thibault P, Meloche S. Activation loop phosphorylation of ERK3/ERK4 by group I p21-activated kinases (PAKs) defines a novel PAK-ERK3/4-MAPK-activated protein kinase 5 signaling pathway. J Biol Chem. 2011 Feb 25;286(8):6470-8. doi: 10.1074/jbc.M110.181529. Epub 2010, Dec 22. PMID:21177870 doi:http://dx.doi.org/10.1074/jbc.M110.181529
