huRANKL(TNFSF11) Mouse
製品名
huRANKL(TNFSF11) Mouse
製品ID
C002107
系統名
C57BL/6Cya-Tnfsf11tm1(hTNFSF11)/Cya
背景情報
C57BL/6Cya
状況
このマウス系統を論文で使用する場合は、「huRANKL(TNFSF11) Mouse（カタログ番号C002107）はサイアジェンから購入しました。」と引用してください。
製品タイプ
年齢
遺伝子型
性別
数量
遺伝子名
遺伝子別名
ODF, OPGL, sOdf, CD254, OPTB2, RANKL, TNLG6B, TRANCE, hRANKL2
NCBI ID
染色体
Chr 13
MGI ID
さらに
系統詳細
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.
参考文献
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.
系統作製戦略
The mouse Tnfsf11 endogenous extracellular domain was replaced with the human TNFSF11 extracellular domain.
Figure 1. Gene editing strategy of huRANKL(TNFSF11) mice.
適用分野
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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