Scaffolding protein that enhances integrin activation mediated by TLN1 and/or TLN2, but activates integrins only weakly by itself. Binds to membranes enriched in phosphoinositides. Enhances integrin-mediated cell adhesion onto the extracellular matrix and cell spreading; this requires both its ability to interact with integrins and with phospholipid membranes. Required for the assembly of focal adhesions. Participates in the connection between extracellular matrix adhesion sites and the actin cytoskeleton and also in the orchestration of actin assembly and cell shape modulation. Plays a role in the TGFB1 and integrin signaling pathways. Stabilizes active CTNNB1 and plays a role in the regulation of transcription mediated by CTNNB1 and TCF7L2/TCF4 and in Wnt signaling (By similarity). Required for normal embryonic development, including normal heart morphogenesis and normal angiogenesis. Colocalizes with actin stress fibers at cell-ECM focal adhesion sites. Colocalizes with integrins at lamellipodia at the leading edge of spreading cells. Binds to membranes that contain phosphatidylinositides (By similarity). The FERM domain is not correctly detected by PROSITE or Pfam techniques because it contains the insertion of a PH domain. The PH domain binds phospholipids. Binds preferentially phosphatidylinositol-3,4,5-trisphosphate, and has lower affinity for phosphatidylinositol-4,5-bisphosphate (By similarity). The N-terminal region displays a ubiquitin-type fold and mediates interaction with membranes containing negatively charged phosphatidylinositol phosphate via a surface enriched in positively charged residues. Morpholino knockdown results in severe defects in embryonic development. Nearly all embryos display pericardial edema. Most embryos display abnormal body shape and size, defects in heart morphogenesis, impaired mobility, and die at about 7 dpf. The embryonic cardiac muscle and skeletal muscle show defects in the association of the actin-myosin myofibers with the myocyte membrane (PubMed:18174465). Likewise, morpholino knockdown results in defective angiogenesis, with abnormally short and thin vessels and very little blood flow (PubMed:21378273). Belongs to the kindlin family.