Correct spelling for the English word "RANKL" is [ɹˈaŋkə͡l], [ɹˈaŋkəl], [ɹ_ˈa_ŋ_k_əl] (IPA phonetic alphabet).
RANKL, also known as Receptor Activator of Nuclear Factor Kappa-B Ligand, is a protein involved in the regulation of bone remodeling and immune function. It is a member of the tumor necrosis factor (TNF) superfamily and is primarily produced by osteoblasts, immune cells such as T cells and B cells, and dendritic cells. RANKL functions as a key signaling molecule in the process of bone resorption, where it binds to its receptor, RANK, found on the surface of osteoclasts, the cells responsible for breaking down bone tissue.
The binding of RANKL to RANK triggers a cascade of signaling events leading to the differentiation, activation, and survival of osteoclasts, promoting bone resorption. This process is critical for maintaining bone structure and turnover, as well as for the regulation of calcium homeostasis. Dysregulation of RANKL expression or signaling can result in bone diseases such as osteoporosis and rheumatoid arthritis.
In addition to its role in bone metabolism, RANKL also plays a crucial role in immune function. It is involved in the development and activation of T and B cells, as well as the interaction between immune cells and dendritic cells. By binding to its receptor, RANKL modulates immune responses, including the activation and differentiation of immune cells.
Manipulation of RANKL signaling has been a therapeutic target for various bone disorders, and RANKL inhibitors have been developed for the treatment of osteoporosis and other bone-related diseases.