a TKL kinase of the LISK family which mediates Rho signaling to cytoskeleton. Contains two N-terminal LIM motifs. Phosphorylated and activated by PAK1 and ROCK, downstream effectors of Rho. May be involved in brain development. Phosphorylates and inactivates the actin binding/depolymerizing factor cofilin and induces actin cytoskeletal changes. The LIM domain interacts with the cytoplasmic domain of NRG1. Binds ROCK1. Interacts with slingshot 1. Overexpressed in prostate tumors and prostate and breast cancer cell lines; manipulation of activity correlates with invasiveness in breast and prostate cancer models. Located within the 7q11.2 amplicon associated with metastatic prostate cancer. Loss of one copy of LIMK1 is the likely cause of visuospatial cognition defects seen in small chromosomal deletions associated with dominant Williams-Beuren syndrome Three splice variant have been identified. Note: This description may include information from UniProtKB.
Protein type: Protein kinase, TKL; Protein kinase, Ser/Thr (non-receptor); Kinase, protein; EC 188.8.131.52; TKL group; LISK family; LIMK subfamily
Molecular Function: protein serine/threonine kinase activity; protein binding; zinc ion binding; protein heterodimerization activity; heat shock protein binding; ATP binding; protein kinase activity
Biological Process: nervous system development; axon guidance; positive regulation of axon extension; negative regulation of ubiquitin-protein ligase activity; innate immune response; positive regulation of actin filament bundle formation; actin cytoskeleton organization and biogenesis; signal transduction; protein amino acid phosphorylation; Rho protein signal transduction
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.