Gly 64-Asp245, with N-terminal Avi Tag & Human IgG1 Fc GLNDIFEAQKIEWHEPKSSDKTHTCPPCPAPELLGGPSVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNSTYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDELTKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQQGNVFSCSVMHEALHNHYTQKSLSLSPGKGGGSGGGSGGGSGSQHIRAEKAMVDGSWLDLAKRSKLEAQPFAHLTINATDIPSGSHKVSLSSWYHDRGWGKISNMTFSNGKLIVNQDGFYYLYANICFRHHETSGDLATEYLQLMVYVTKTSIKIPSSHTLMKGGSTKYWSGNSEFHFYSINVGGFFKLRSGEEISIEVSNPSLLDPDQDATYFGAFKVRDID
1. Paul R. Odgren, Nacksung Kim, Carole A. MacKay, April Mason-Savas, Yongwon Choi &Sandy C. Marks, Jr.: The Role of RANKL (TRANCE/TNFSF11), a Tumor Necrosis Factor Family Member, in Skeletal Development: Connective Tissue Research, Volume 44, 2003, Pages 264-271.
RANKL (also known as TRANCE or OPGL) is a member of the TNF ligand superfamily. RANKL is produced by T cells, mammary epithelial cells and endothelial cells. RANKL, through its ability to stimulate osteoclast formation and activity, is a critical mediator of bone resorption and overall bone density. RANK and RANKL are key regulators of bone remodeling and regulate T cell/dendritic cell communications, and lymph node formation.RANK-RANKL signaling not only activates a variety of downstream signaling pathways required for osteoclast development, but crosstalk with other signaling pathways also fine-tunes bone homeostasis both in normal physiology and disease.
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