PAK3
PAK3 (p21 (RAC1) activated kinase 3, also known as hPAK3, bPAK, MRX30 and MRX47) is a serine/threonine kinase and a downstream effector of the small GTPases CDC42 and RAC1. It contributes to cytoskeleton regulation, cell migration and the formation of dendritic spines and synapses. Browse Assay Genie's current range of PAK3 research reagents below, or read on for the biology behind the target.
PAK3 is a serine/threonine protein kinase that acts in several signalling pathways, including those controlling cytoskeleton organisation, cell migration and cell cycle regulation. It is a downstream effector of the small GTPases CDC42 and RAC1. Binding of the active GTPases causes a conformational change, followed by autophosphorylation on several serine and/or threonine residues. Active PAK3 phosphorylates MAPK4 and MAPK6 and activates the downstream target MAPKAPK5, a regulator of F-actin polymerisation and cell migration. It also phosphorylates TNNI3 (troponin I), modulating the calcium sensitivity and relaxation kinetics of thin myofilaments.
In the nervous system, PAK3 has a role in dendritic spine morphogenesis, synapse formation and synaptic plasticity, and it may also be involved in early neuronal development. In hippocampal neurons it is necessary for the formation of dendritic spines and excitatory synapses. This depends on its kinase activity and may operate through regulation of actomyosin contractility, via phosphorylation of myosin II regulatory light chain. The protein localises to the cytoplasm. It belongs to the protein kinase superfamily, STE Ser/Thr protein kinase family, STE20 subfamily, and is a member of the p21 (RAC1) activated kinase family. Researchers studying the PAK3 gene or PAK3 protein will find mouse and rat orthologs, both named Pak3.
The gene has been called p21 (CDKN1A)-activated kinase 3 and p21 protein (Cdc42/Rac)-activated kinase 3. Its earlier name, mental retardation, X-linked 47, reflects its disease link: defects in the gene cause a non-syndromic form of X-linked intellectual disability. Alternatively spliced transcript variants encoding different isoforms have been identified.
PAK3 is linked to rapid cytoskeletal reorganisation in dendritic spines associated with synaptic plasticity.
Defects in PAK3 cause a non-syndromic form of X-linked intellectual disability and the kinase may act in early neuronal development.
PAK3 is activated by binding of active CDC42 and RAC1, making it a model effector for studying GTPase signalling.
PAK3 phosphorylates MAPK4 and MAPK6 and activates MAPKAPK5, a regulator of F-actin polymerisation and cell migration.
PAK3 is a serine/threonine kinase activated by CDC42 and RAC1. It regulates the cytoskeleton, cell migration and cell cycle signalling, and it supports dendritic spine formation, excitatory synapse formation and synaptic plasticity in neurons, partly through phosphorylation of myosin II regulatory light chain.
PAK3 is also called hPAK3, bPAK, MRX30 and MRX47. Former names include p21 (CDKN1A)-activated kinase 3 and mental retardation, X-linked 47. UniProt lists the protein as serine/threonine-protein kinase PAK 3. Alternative splicing gives transcript variants that encode different isoforms.
Defects in PAK3 cause a non-syndromic form of X-linked intellectual disability. Mouse and rat both have an ortholog named Pak3. For any product, check the datasheet for its validated reactivity.
Other members of the p21 (RAC1) activated kinase family with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt O75914; product specifications from Assay Genie datasheets.