RECK
RECK (reversion inducing cysteine rich protein with kazal motifs, also known as hRECK and ST15) is a membrane-anchored glycoprotein that inhibits matrix metalloproteinases and acts as a Wnt7-specific coactivator of canonical Wnt signalling. Browse Assay Genie's current range of RECK research reagents below, or read on for the biology behind the target.
RECK has two well-described roles. It acts as a serine protease inhibitor-like regulator of extracellular proteolysis: it negatively regulates matrix metalloproteinase-9 (MMP9) by suppressing MMP9 secretion and by directly inhibiting its enzymatic activity. It also inhibits the metalloproteinase activity of MMP2, MMP14 (MT1-MMP) and ADAM10. In normal cells, this membrane-anchored protein is considered a negative regulator of MMP9, a key enzyme in tumour invasion and metastasis.
RECK also functions in signalling. Together with ADGRA2, it allows brain endothelial cells to respond selectively to Wnt7 signals (WNT7A or WNT7B). RECK acts as a Wnt7-specific coactivator of canonical Wnt signalling by decoding Wnt ligands: it binds the disordered linker region of Wnt7, which gives ligand selectivity. ADGRA2 then delivers RECK-bound Wnt7 to frizzled by assembling a higher-order RECK-ADGRA2-Fzd-LRP5-LRP6 complex. Through this mechanism RECK is required for central nervous system (CNS) angiogenesis and regulation of the blood-brain barrier.
The RECK gene encodes a cysteine-rich, extracellular glycoprotein with protease inhibitor-like domains, and it belongs to the RECK family. Its expression is strongly suppressed in many tumours and in cells transformed by various oncogenes, which is reflected in its name. Several transcript variants encoding different isoforms have been reported. The mouse ortholog is Reck, and the protein localises to the cell membrane.
RECK expression is suppressed in many tumours, and it negatively regulates MMP9, an enzyme central to tumour invasion and metastasis.
RECK inhibits MMP2, MMP9, MMP14 (MT1-MMP) and ADAM10, making it a useful focus for studying metalloproteinase control.
RECK decodes Wnt7 ligands and assembles a complex with ADGRA2, frizzled, LRP5 and LRP6 to drive canonical Wnt signalling.
RECK is required for CNS angiogenesis and blood-brain barrier regulation through Wnt7-specific responses in brain endothelial cells.
RECK is a membrane-anchored protein that inhibits MMP9 by suppressing its secretion and directly blocking its activity, and also inhibits MMP2, MMP14 and ADAM10. It also acts with ADGRA2 as a Wnt7-specific coactivator, supporting CNS angiogenesis and blood-brain barrier regulation.
RECK is also known as hRECK and ST15, and its full name is reversion-inducing cysteine-rich protein with Kazal motifs. NCBI Gene reports several transcript variants that encode different isoforms. Check the datasheet of any product for its validated reactivity.
RECK expression is strongly suppressed in many tumours and in cells transformed by oncogenes, consistent with its role as a negative regulator of MMP9, which is involved in invasion and metastasis. A mouse ortholog, Reck, has been identified.
Metalloproteinases, Wnt ligands, Wnt co-receptors and ADGRA2, which act alongside RECK in matrix regulation and Wnt7 signalling.
Gene and protein annotations from HGNC, NCBI Gene and UniProt O95980; product specifications from Assay Genie datasheets.