RANKL Protein (AA 64-245)

Catalog No. ABIN2666867

This Recombinant RANKL protein is expressed in HEK-293 Cells.

Quick Overview for RANKL Protein (AA 64-245) (ABIN2666867)

Target: RANKL (TNFSF11) (Tumor Necrosis Factor (Ligand) Superfamily, Member 11 (TNFSF11))

Protein Type: Recombinant

Biological Activity: Active

Origin: Human

Source: HEK-293 Cells

Application: ELISA, Flow Cytometry (FACS)

Purity: > 95 % , as determined by Coomassie stained SDS-PAGE.

Product Details

Protein Characteristics: AA 64-245

Sterility: 0.22 μm filtered

Endotoxin Level:

Less than 0.01 ng per μg cytokine as determined by the LAL method.

Application Details

Application Notes: Optimal working dilution should be determined by the investigator.

Comment:

Biological activity: Bioactivity was measured by its property to induce osteoclast differentiation in RAW264.7 cells in the presence of 2.5 μg/ml of anti-His tag antibody (Cat. No. 652501).

Restrictions: For Research Use only

Handling

Format: Liquid

Reconstitution: For maximum results, quick spin vial prior to opening. Stock solutions should be prepared at no less than 10 μg/mL in sterile buffer (PBS, HPBS, DPBS, and EBSS) containing carrier protein such as 1 % BSA or HSA. After dilution, the cytokine can be stored between 2 °C and 8 °C for one month or from -20 °C to -70 °C for up to 3 months.

Buffer: 0.22 μm filtered protein solution is in PBS pH 6.5.

Handling Advice: Avoid repeated freeze/thaw cycles.

Storage: -20 °C

Storage Comment: Unopened vial can be stored between 2°C and 8°C for three months, at -20°C for six months, or at -70°C for one year.

Target Details

Target: RANKL (TNFSF11) (Tumor Necrosis Factor (Ligand) Superfamily, Member 11 (TNFSF11))

Alternative Name: TRANCE

Background: Human TRANCE gene, also known as RANKL, encodes a type II membrane protein of 317 amino acids with a predicted molecular mass of 35.4 kD. RANKL is cleaved to produce a soluble form with biological activity. The shedding of membrane-bound RANKL appears to be mediated by expression of matrix metalloproteinase 14 (MMP14) and ADAM10. Suppression of MMP14 in primary osteoblasts increased membrane-bound RANKL and promoted osteoclastogenesis in cocultures with macrophages. Therefore, RANKL shedding seems to be an important process that downregulates local osteoclastogenesis. Conversely, increased production of RANKL by osteoblastic cells leads to osteoclast differentiation, activation, and survival, which results in increased bone resorption. Binding of RANKL to its receptor RANK activates TNF receptor-associated factor 6 (TRAF6), which is linked to downstream pathways including NF-κB, c-jun N-terminal kinase (JNK), and Src. TRAF6 in particular has been shown to be necessary for the differentiation of osteoclastic cells by enhancing Src kinase, essential for osteoclast function. Activation of JNK and NF-κB by RANKL induces the expression of IL-1, IL-6, IL-12, and IL-15 in dendritic cells. In addition, RANKL stimulates proliferation, adhesion, and IL-7 expression of thymic epithelial cells. RANKL can mediate bone loss in arthritis and periodontal disease.

Molecular Weight: The 203 amino acid recombinant protein has a predicted molecular mass of approximately 22.7 kDa. The DTT-reduced and non-reduced protein migrate at approximately 36-40 kDa by SDS-PAGE. The N-terminal amino acid is His.

Pathways: NF-kappaB Signaling