RANK/TNFRSF11A Protein, Human (HEK293, His)

RANK (TNFRSF11A) is a receptor activator of nuclear factor κB (NF-κB), which is involved in bone metabolism and immune system function. RANK is mainly expressed by osteoblasts/stromal cells, and is associated with the formation of giant cell tumor of bone (GCTBs) ^[1]. RANK combined with RANKL ligand activated the RANKL/RANK/ OPG system to regulate bone resorption ^[2]. RANKL/RANK is also a regulator of dendritic cell (DC)-T cell interaction, which is associated with mammary epithelial formation and central nervous system thermoregulation in lactating female ^[3][4]. RANK/TNFRSF11A Protein, Human (HEK293, His) has 183 amino acids (I30-P212), produced by HEK293 cells with C-terminal 6*His-tag.

RANK (TNFRSF11A), is the receptor activator of nuclear factor-κB (NF-κB), has originally been described to play key roles in bone metabolism and the immune system. RANK belongs to tumor necrosis factor receptor superfamily, acts function during osteoclasts differentiation and activation. RANK expressed by osteoblast/stromal cells, ubiquitous expression with high levels in skeletal muscle, thymus, liver, colon, small intestine and adrenal gland. However, osteoblast typically are present in large numbers in giant cell tumors of bone (GCTBs), suggesting the affect of expressing factors in tumors that stimulate osteoclasts precursor recruitment and differentiation^[1]. RANK binds RANKL, the receptor activator of NF-κB ligand, to trigger RANKL/RANK/osteoprotegerin (OPG) system to regulate bone resorption. Specifically, the RANKL/RANK signaling pathway promotes the formation of multicellular osteoclast precursors and ensures the activation and survival of multicellular osteoclasts under normal bone remodeling and various pathological conditions. OPG protects bone from excessive bone resorption by competitively binding to RANKL and hindering RANK binding to RANKL^[2]. In addition to RANK's contribution to bone metabolism, the RANKL/RANK system is also involved in dendritic cell (DC)-T cell interactions. In rheumatoid synovium and lymph node pairs, the expression levels of RANK and RANKL can be used as markers to determine the interaction between dendritic cells and T cells^[3]. Moreover, RANKL-RANK system is critical in the formation of mammary epithelia in lactating females and the thermoregulation of the central nervous system. As them under the tight control of the female sex hormones estradiol and progesterone, RANKL-RANK causes osteoporosis in postmenopausal women when circulating female sex hormones decrease. Furthermore, RANKL-RANK signaling also plays a critical role in other bone pathologies, bone metastasis or hormone-driven breast cancer^[4].

Human

HEK293

C-6*His

Q9Y6Q6 (I30-P212)

8792  [NCBI]

Extracellular Domain

IAPPCTSEKHYEHLGRCCNKCEPGKYMSSKCTTTSDSVCLPCGPDEYLDSWNEEDKCLLHKVCDTGKALVAVVAGNSTTPRRCACTAGYHWSQDCECCRRNTECAPGLGAQHPLQLNKDTVCKPCLAGYFSDAFSSTDKCRPWTNCTFLGKRVEHHGTEKSDAVCSSSLPARKPPNEPHVYLP

Approximately 25-30 kDa, based on SDS-PAGE under reducing conditions.

≥ 95%, as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.

• [1]. Roux S, et al. RANK (receptor activator of nuclear factor kappa B) and RANK ligand are expressed in giant cell tumors of bone. Am J Clin Pathol. 2002 Feb;117(2):210-6.  [Content Brief]

  [2]. Boyce BF, et al. Biology of RANK, RANKL, and osteoprotegerin. Arthritis Res Ther. 2007;9 Suppl 1(Suppl 1):S1.  [Content Brief]

  [3]. Page G, et al. RANK and RANKL expression as markers of dendritic cell-T cell interactions in paired samples of rheumatoid synovium and lymph nodes. Arthritis Rheum. 2005 Aug;52(8):2307-12.  [Content Brief]

  [4]. Nagy V, et al. The RANKL-RANK Story. Gerontology. 2015;61(6):534-42.  [Content Brief]