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Rabbit Anti-RANK/HRP Conjugated antibody (bs-7343R-HRP)
訂購熱線:400-901-9800
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訂購QQ:  400-901-9800
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價
產(chǎn)品編號 bs-7343R-HRP
英文名稱 Rabbit Anti-RANK/HRP Conjugated antibody
中文名稱 辣根過氧化物酶標記的核轉錄因子NF-κB受體/核因子kB受體活化因子抗體
別    名 TNFRSF11A; CD 265; CD265; CD265 antigen; Activator of NFKB; EOF; FEO; mRANK; NFKB activator; ODFR; OFE; Osteoclast differentiation factor receptor; PDB 2; Receptor activator of NF KB; receptor activator of nuclear factor kappa B; TNFRSF 11A; TNFSF11; TRANCE R; RANK receptor; TNR11_HUMAN.  
規(guī)格價格 100ul/2980元 購買        大包裝/詢價
說 明 書 100ul  
研究領域 腫瘤  細胞生物  轉錄調(diào)節(jié)因子  細胞表面分子  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應 (predicted: Human, Mouse, Rabbit, Sheep, )
產(chǎn)品應用 ELISA=1:100-1000 IHC-P=1:50-200 IHC-F=1:50-200 ICC=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 63kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human RANK/CD265
亞    型 IgG
純化方法 affinity purified by Protein A
儲 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件 Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
產(chǎn)品介紹 background:
CD265 is a member of the tumor necrosis factor receptor (TNFR) family. Human and murine CD265 share 81% amino acid identity in their extracellular domains. CD265 is widely expressed, with highest levels in skeletal muscle, thymus, liver, colon, small intestine and adrenal gland. CD265 is also expressed in dendritic cells. RANK and RANK ligand (RANKL) are important regulators of interactions between T cells and dendritic cells. RANK is the essential signaling receptor for osteoclast differentiation factor in osteoclastogenesis. Multiple tumor necrosis factor receptor-associated factors (TRAFs) are involved in the signaling of CD265. TRANCE (TNF-related activation-induced cytokines, also known as RANK ligand, osteoprotegerin ligand and osteoclast differentiation factor) is the ligand for CD265. The biological functions mediated by RANK include activation of NFkappaB and cjun N-terminal kinase, enhancement of T cell growth and dendritic cell function, induction of osteoclastogenesis and lymph node organogenesis. The soluble form of CD265 is able to block TRANCE induced biological activity. The binding of anti-CD265 to cell surface CD265 triggers signal transduction and induces CD265 mediated bioactivity.

Function:
Receptor for TNFSF11/RANKL/TRANCE/OPGL; essential for RANKL-mediated osteoclastogenesis. Involved in the regulation of interactions between T-cells and dendritic cells.

Subcellular Location:
Membrane.

Tissue Specificity:
Ubiquitous expression with high levels in skeletal muscle, thymus, liver, colon, small intestine and adrenal gland.

DISEASE:
Defects in TNFRSF11A are the cause of familial expansile osteolysis (FEO) [MIM:174810]. FEO is a rare autosomal dominant bone disorder characterized by focal areas of increased bone remodeling. The osteolytic lesions develop usually in the long bones during early adulthood. FEO is often associated with early onset deafness and loss of dentition. Defects in TNFRSF11A are a cause of Paget disease of bone type 2 (PDB2) [MIM:602080]; also known as familial Paget disease of bone. PDB2 is a bone-remodeling disorder with clinical similarities to FEO. Unlike FEO, however, affected individuals have involvement of the axial skeleton with lesions in the spine, pelvis and skull.

Similarity:
Contains 4 TNFR-Cys repeats.

Database links:

Entrez Gene: 8792 Human

Entrez Gene: 21934 Mouse

Omim: 603499 Human

SwissProt:  Human

SwissProt: O35305 Mouse

Unigene: 204044 Human

Unigene: 6251 Mouse



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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