Recombinant Human Serine/threonine-protein kinase PAK 3 (PAK3)

Uniprot Id

O75914

Target Species

Human

Target Name

PAK3

Target Full Name

Serine/threonine-protein kinase PAK 3

Target Function

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. In hippocampal neurons, necessary for the formation of dendritic spines and excitatory synapses; this function is dependent on kinase activity and may be exerted by the regulation of actomyosin contractility through the phosphorylation of myosin II regulatory light chain (MLC).

Target Involvement

Mental retardation, X-linked 30 (MRX30)

Target Subcellular Location

Cytoplasm.

Target Protein Families

Protein kinase superfamily, STE Ser/Thr protein kinase family, STE20 subfamily

Target Tissue Specificity

Restricted to the nervous system. Highly expressed in postmitotic neurons of the developing and postnatal cerebral cortex and hippocampus.

Target Synonyms

PAK3; OPHN3; Serine/threonine-protein kinase PAK 3; EC 2.7.11.1; Beta-PAK; Oligophrenin-3; p21-activated kinase 3; PAK-3

Target Background

The protein encoded by this gene is a serine-threonine kinase and forms an activated complex with GTP-bound RAS-like (P21), CDC2 and RAC1. This protein may be necessary for dendritic development and for the rapid cytoskeletal reorganization in dendritic spines associated with synaptic plasticity. Defects in this gene are the cause of a non-syndromic form of X-linked intellectual disability. Alternatively spliced transcript variants encoding different isoforms have been identified.