Recombinant Rabbit monoclonal primary
PAK3 Recombinant Rabbit Monoclonal Antibody [JE57-39] (ET7111-35)
Synthetic peptide within n-terminal human pak3.
Rat brain tissue lysates, F9.
Store at +4Á¾ after thawing. Aliquot store at -20Á¾. Avoid repeated freeze / thaw cycles.
1*TBS (pH7.4), 0.05% BSA, 40% Glycerol. Preservative: 0.05% Sodium Azide.
Protein A affinity purified.
Beta PAK antibody; bPAK antibody; CDKN1A antibody; hPAK3 antibody; Mental retardation X linked 30 antibody; MRX30 antibody; MRX47 antibody; Oligophrenin 3 antibody; OPHN3 antibody; p21 (CDKN1A) activated kinase 3 antibody; p21 activated kinase 3 antibody; p21 CDKN1A activated kinase 3 antibody; P21 protein (Cdc42/Rac) activated kinase 3 antibody; PAK-3 antibody; PAK3 p21 protein (Cdc42/Rac)-activated kinase 3 antibody; PAK3beta antibody; Pak65alpha antibody; Pak65beta antibody; Serine threonine protein kinase PAK 3 antibody; Stk4 antibody
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. 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. 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.