The Tolloid-like 1 (TLL1) protein, a member of the astacin family of zinc-dependent metalloproteases, plays a critical role in extracellular matrix (ECM) remodeling and growth factor activation. It shares structural homology with BMP-1 (bone morphogenetic protein-1) and is involved in proteolytic processing of precursors such as procollagen and prolysyl oxidase, as well as latent TGF-β binding proteins. TLL1 is essential in embryonic development, particularly in heart formation, neural tube closure, and tissue morphogenesis, as demonstrated by knockout mouse models exhibiting severe cardiovascular defects.
In disease contexts, TLL1 dysregulation has been linked to fibrosis, cancer progression, and cardiovascular disorders. For example, elevated TLL1 expression correlates with hepatic fibrosis by promoting ECM deposition and activating pro-fibrotic signaling pathways. In cancer, TLL1 may facilitate tumor invasion through ECM degradation and growth factor activation.
TLL1 antibodies are valuable tools for detecting TLL1 expression in tissues or cell lines via techniques like Western blot, immunohistochemistry, or immunofluorescence. They also aid in studying TLL1's functional mechanisms in development and disease. Recent research explores TLL1 as a potential therapeutic target, with neutralizing antibodies being investigated to inhibit its proteolytic activity in fibrotic or metastatic models. However, its dual roles in tissue homeostasis and pathology necessitate context-specific therapeutic strategies.