RANKL/TNFSF11 蛋白, Mouse (HEK293, Fc)

RANKL (TNFSF11), a type II transmembrane protein, is a receptor activator of NF-κB (RANK) ligand. RANKL is an activator of RANK. When binding to RANK, it induces the differentiation of monocyte/macrophage-lineage cells into osteoclasts and leads to osteoclast precursor maturation. RANKL is critical for osteoclasts maturation, bone modeling, and bone remodeling, as well as the development of lymph nodes (LNs). RANKL/TNFSF11 Protein, Mouse (HEK293, Fc) is a recombinant mouse RANKL (R72-D316) with N-terminal hFc tag, which is produced in HEK293^[1][2].

RANKL (TNFSF11) 属于 TNF 家族。RANKL 是一种 II 型跨膜蛋白，是 NF-κB (RANK) 配体的受体激活剂。RANKL 是 RANK 的激活剂。RANKL 与 RANK 结合，诱导单核细胞/巨噬细胞谱系细胞分化为破骨细胞，并导致破骨细胞前体成熟。在骨组织中，RANKL 由成骨细胞、骨细胞和免疫细胞表达，尤其是在成骨细胞和骨细胞中表达^[1]。RANKL 也由 T 细胞表达，可增加树突状细胞的增殖和存活^[2]。在小鼠中，RANKL/RANK 信号传导通过 Toll 样受体信号传导通路减轻缺血性脑部的炎症^[4]。
RANKL 由细胞质结构域 (1-47)、螺旋结构域 (48) 组成-68) 和胞外结构域 (69-317)。当基质金属蛋白酶（MMP3 或 7）和 ADAM^[1][3] 等酶裂解时，可溶性链 (140-317) 被释放。
RANKL 对于破骨细胞成熟、骨建模和骨重塑以及淋巴结 (LN) 的发育至关重要^[1]。

RANKL (mouse, 3 ng/mL, 4 days) induces osteoclast differentiation from RAW264.7 cells, and can be inhibited by Resveratrol^[5].
RANKL (mouse,1 ng/mL, -3 h) induces NF-κB activation in murine hepatocyte cell line (AML-12) ^[6].

RANKL (mouse, i.c.v., 5 ng in 2 μL) reduces IL-1β, MCP-1, IL-6 and TNFα expression in WT mice^[4].
RANKL (mouse, i.p., 1-1 μg) protects against hepatic ischemia/reperfusion liver injury in mice^[6].

1.Measured by its ability to induce osteoclast differentiation of RAW 264.7 mouse leukemia cells of monocyte macrophage. The ED₅₀ for this effect is ≤1.280 ng/mL, corresponding to a specific activity is ≥7.81×10⁵ units/mg.
2.Immobilized mouse Fc-TNFSF11 at 10 μg/mL (100 μl/well) can bind biotinylated human TNFRSF11B-His , The EC₅₀ of biotinylated human TNFRSF11B-His is 0.07-0.17 μg/mL.

Mouse

HEK293

N-hFc

AAC40113.1/ O35235-1(R72-D316)

21943  [NCBI]

RAQMDPNRISEDSTHCFYRILRLHENAGLQDSTLESEDTLPDSCRRMKQAFQGAVQKELQHIVGPQRFSGAPAMMEGSWLDVAQRGKPEAQPFAHLTINAASIPSGSHKVTLSSWYHDRGWAKISNMTLSNGKLRVNQDGFYYLYANICFRHHETSGSVPTDYLQLMVYVVKTSIKIPSSHNLMKGGSTKNWSGNSEFHFYSINVGGFFKLRAGEEISIQVSNPSLLDPDQDATYFGAFKVQDID

Approximately 56-70 kDa due to the glycosylation.

• 
  Greater than 90% as determined by reducing SDS-PAGE.

无菌粉末

Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4 or PBS, pH 7.4, 5% trehalose, 5% mannitol and 0.01% Tween80.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O.

Stored at -20°C for 2 years. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [1]. Ono T, et al. RANKL biology: bone metabolism, the immune system, and beyond. Inflamm Regen. 2020 Feb 7;40:2.  [Content Brief]

  [2]. Li B, et al. Roles of the RANKL-RANK Axis in Immunity-Implications for Pathogenesis and Treatment of Bone Metastasis. Front Immunol. 2022 Mar 21;13:824117.  [Content Brief]

  [3]. Tobeiha M, et al. RANKL/RANK/OPG Pathway: A Mechanism Involved in Exercise-Induced Bone Remodeling. Biomed Res Int. 2020 Feb 19;2020:6910312.  [Content Brief]

  [4]. Shimamura M, et al. OPG/RANKL/RANK axis is a critical inflammatory signaling system in ischemic brain in mice. Proc Natl Acad Sci U S A. 2014 Jun 3;111(22):8191-6.  [Content Brief]

  [5]. He X, et al. Resveratrol prevents RANKL-induced osteoclast differentiation of murine osteoclast progenitor RAW 264.7 cells through inhibition of ROS production. Biochem Biophys Res Commun. 2010 Oct 22;401(3):356-62.  [Content Brief]