Involved in the control of cytoskeleton formation by regulating actin polymerization. Inhibits actin fiber formation and cell migration. Inhibits RhoA activity; the function involves phosphorylation through PI3K/Akt signaling and may depend on the competetive interaction with 14-3-3 adapter proteins to sequester them from active complexes. Inhibits the formation of lamellipodia but not of filopodia; the function may depend on the competetive interaction with BAIAP2 to block its association with activated RAC1. Inhibits fibronectin-mediated cell spreading; the function is partially mediated by BAIAP2. Inhibits neurite outgrowth. Involved in the establishment and persistence of cell polarity during directed cell movement in wound healing. In the nucleus, is involved in beta-catenin-dependent activation of transcription. Potential tumor suppressor for renal cell carcinoma. Defects in KANK1 are the cause of cerebral palsy spastic quadriplegic type 2 (CPSQ2). A non-progressive disorder of movement and/or posture resulting from defects in the developing central nervous system. Affected individuals manifest congenital hypotonia evolving over the first year to spastic quadriplegia with accompanying transient nystagmus and varying degrees of mental retardation. Neuroimaging shows brain atrophy and ventriculomegaly. 2 isoforms of the human protein are produced by alternative promoter. Note: This description may include information from UniProtKB.
Molecular Function: beta-catenin binding; protein binding
Biological Process: negative regulation of actin filament polymerization; negative regulation of cell migration; negative regulation of insulin receptor signaling pathway; negative regulation of Rho protein signal transduction; positive regulation of Wnt receptor signaling pathway