Functions together with ADGRA2 to enable brain endothelial cells to selectively respond to Wnt7 signals (WNT7A or WNT7B) (PubMed:28803732). Plays a key role in Wnt7-specific responses: required for central nervous system (CNS) angiogenesis and blood-brain barrier regulation (PubMed:26658478, PubMed:28803732). Acts as a Wnt7-specific coactivator of canonical Wnt signaling by decoding Wnt ligands: acts by interacting specifically with the disordered linker region of Wnt7, thereby conferring ligand selectivity for Wnt7 (By similarity). ADGRA2 is then required to deliver RECK-bound Wnt7 to frizzled by assembling a higher-order RECK-ADGRA2-Fzd-LRP5-LRP6 complex (By similarity). Also acts as a serine protease inhibitor: negatively regulates matrix metalloproteinase-9 (MMP9) by suppressing MMP9 secretion and by direct inhibition of its enzymatic activity (PubMed:11747814). Also inhibits metalloproteinase activity of MMP2 and MMP14 (MT1-MMP) (PubMed:11747814). Interacts (via knot repeats) with WNT7A (via disordered linker region); the interaction is direct (By similarity). Interacts (via knot repeats) with WNT7B (via disordered linker region); the interaction is direct (By similarity). Interacts with ADGRA2; the interaction is direct (PubMed:28803732). Interacts with MMP9 (By similarity). In 10.5 dpc embryos, widely expressed in mesenchymal tissues and is relatively abundant in the marginal zone of the neural tube and large blood vessels such as the aorta. The Kazal-like domains mediate the serine protease inhibitor activity. Embryonic lethality around 10.5 dpc, caused by reduced tissue integrity, arrested vasculogenesis and precocious neuronal differentiation (PubMed:11747814). Conditional knockout mice lacking Reck in endothelial cells show central nervous system (CNS) angiogenesis defects, characterized by moderate hemorrhages in the forebrain and vascular malformations in the cortex (PubMed:26658478, PubMed:28803732). Conditional deletion in endothelial cells also cause blood-brain barrier defects in neonates (PubMed:28803732). Phenotypes are caused by impaired beta-catenin-dependent signaling (PubMed:28803732). Belongs to the RECK family.