LOX is a copper-dependent amine oxidase enzyme that executes post-translational oxidative deamination on peptidyl lysine residues in precursors of fibrous collagen and elastin. LOX is secreted into the extracellular environment in an inactive form, where it is processed into an active form. Its activity is crucial for maintaining both the tensile and elastic properties of connective tissue residing within skeletal, pulmonary, and cardiovascular systems. Furthermore, its expression is highly regulated during normal development and uncontrolled expression or activity has been documented in a wide range of predominantly ECM diseases. These diseases include, but are not limited to, myocardial ischemia/heart failure, atherosclerosis, scleroderma, liver cirrhosis, glaucoma, Alzheimer's/non-Alzheimer's dementia, and Wilson's disease. In addition to its matrix modifying functions, LOX is also heavily implicated as a tumor suppressor.
Contente’s group used a LOX antibody to better understand the dynamic interplay between the propeptide and mature forms of LOX localized between the subcellular and extracellular compartments of the cell1. Studies out of UCSF with a LOX antibody was used to monitor GATA3 function in breast cancer tumor microenvironment and the findings were published in Nature Cell Biology2. Based on those studies, it appears that GAT3 promotes differentiation, suppresses tumor metastasis, and induces miR-29b through selective downregulation of pro-metastatic regulators such as VEGF and PDGF. Additional studies using a LOX antibody include validation of a novel organ culture system, based on a splashing bioreactor that mimics in vivo microstructure and tissue integrity3. This same research group also used the LOX antibody in follow-up studies demonstrating that their organ culture can be used as an identification tool for early events in serotonergic valve disease and characteristic plaque formation4. Lastly, Desguerre’s group in France also employed a LOX antibody to help validate their induced fibrotic dystrophic model based upon chronic mechanical muscle injuries to generate chronic lesions in hindlimb muscle5.
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