huRANKL(TNFSF11) Mouse
Product Name
huRANKL(TNFSF11) Mouse
Product ID
C002107
Strain Name
C57BL/6Cya-Tnfsf11tm1(hTNFSF11)/Cya
Background
C57BL/6Cya
Status
When using this mouse strain in a publication, please cite “huRANKL(TNFSF11) Mouse (Catalog C002107) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Standard products are sold as live mice derived from cryorecovery or expansion. Frozen materials are available upon request. Pricing and lead times depend on real-time inventory.
Gene Name
TNFSF11
Gene Alias
ODF, OPGL, sOdf, CD254, OPTB2, RANKL, TNLG6B, TRANCE, hRANKL2
NCBI ID
Chromosome
Chr 13 (Human)
MGI ID
Datasheet
Strain Description
The TNFSF11 gene (also known as receptor activator of nuclear factor‑κB ligand, RANKL) encodes a key member of the tumor necrosis factor superfamily. Its expression is broadly distributed across multiple cell types within the bone microenvironment and the immune system, including osteoblasts, osteocytes, bone marrow stromal cells, activated T cells, and certain B cells [1]. The cytokine encoded by this gene exerts its effects by specifically binding to the signaling receptor TNFRSF11A/RANK and the decoy receptor TNFRSF11B/OPG, thereby regulating core biological processes, such as osteoclast differentiation, activation, and bone remodeling, while also participating in lymph node organogenesis, T‑cell–dendritic cell interactions, and mammary gland development [2]. TNFSF11 plays a central role in both bone homeostasis and adaptive immunity: on one hand, it serves as a critical inducer of osteoclast differentiation and activation, mediating bone resorption and calcium–phosphate metabolism [3]; on the other hand, it provides survival and functional signals to immune cells and promotes osteo‑immune crosstalk under inflammatory conditions [4]. Dysregulation of TNFSF11 expression or signaling has been causally linked to multiple human diseases. Loss‑of‑function mutations impair osteoclastogenesis, leading to autosomal recessive osteopetrosis, whereas hyperactivation or aberrant expression of TNFSF11 signaling promotes pathological bone resorption and contributes to conditions such as osteoporosis, rheumatoid arthritis-associated bone erosion, and tumor bone metastasis, including breast and prostate cancer [5-8].
The huRANKL(TNFSF11) mouse is a humanized model constructed via gene-editing technology. The mouse Tnfsf11 endogenous extracellular domain was replaced with the human TNFSF11 extracellular domain. This model can be used for the mechanistic studies of various bone metabolism- and bone immunity-related diseases, including osteoporosis, bone erosion in rheumatoid arthritis, osteopetrosis, and tumor bone metastasis, as well as for the screening, development, and preclinical in vivo evaluation of TNFSF11-targeting antibodies, small molecule inhibitors, and other therapeutic agents.
Reference
Honma M, Ikebuchi Y, Suzuki H. RANKL as a key figure in bridging between the bone and immune system: Its physiological functions and potential as a pharmacological target. Pharmacol Ther. 2021;218:107682.
Zartab, Hamed., Maghsoodloo, Dorian., Parsi-Moud, Abolfazl., Ahmadi, Mohammad Amin., & Rezaei Zadeh Rukerd, Mohammad.. (2025). The RANK-RANKL-OPG axis in dermatological malignancies: A systematic review. International immunopharmacology.
Udagawa N, Koide M, Nakamura M, et al. Osteoclast differentiation by RANKL and OPG signaling pathways. J Bone Miner Metab. 2021;39(1):19-26.
Santamaria JC, Chevallier J, Dutour L, et al. RANKL treatment restores thymic function and improves T cell-mediated immune responses in aged mice. Sci Transl Med. 2024;16(776):eadp3171.
Frattini, Annalisa., Vezzoni, Paolo., Villa, Anna., & Sobacchi, Cristina.. (2007). The Dissection of Human Autosomal Recessive Osteopetrosis Identifies an Osteoclast-Poor Form due to RANKL Deficiency. Cell cycle (Georgetown, Tex.), 6(24), 3027-3033.
Komatsu N, Takayanagi H. Mechanisms of joint destruction in rheumatoid arthritis - immune cell-fibroblast-bone interactions. Nat Rev Rheumatol. 2022;18(7):415-429.
Tenshin, Hirofumi., Delgado-Calle, Jesus., Windle, Jolene J., Roodman, G David., & Chirgwin, John M.. (2024). Osteocytes and Paget's Disease of Bone. Current osteoporosis reports.
Zhang Y, Liang J, Liu P, Wang Q, Liu L, Zhao H. The RANK/RANKL/OPG system and tumor bone metastasis: Potential mechanisms and therapeutic strategies. Front Endocrinol (Lausanne). 2022;13:1063815.
Strain Strategy
The mouse Tnfsf11 endogenous extracellular domain was replaced with the human TNFSF11 extracellular domain.
Figure 1. Gene editing strategy of huRANKL(TNFSF11) mice.
Application Area
Mechanistic studies on bone metabolic and bone immune disorders, including osteoporosis, rheumatoid arthritis‑associated bone erosion, osteopetrosis, and tumor bone metastasis;
Screening, development, and preclinical in vivo evaluation of TNFSF11‑targeting antibodies, small molecule inhibitors, and other therapeutic agents.
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