RANKL Protein (AA 70-244, N-Term)

Catalog No. ABIN2667597

Recombinant RANKL protein expressed in Escherichia coli (E. coli).

Quick Overview for RANKL Protein (AA 70-244, N-Term) (ABIN2667597)

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

Protein Type: Recombinant

Biological Activity: Active

Origin: Human

Source: Escherichia coli (E. coli)

Application: Western Blotting (WB), Immunoprecipitation (IP), Immunofluorescence (IF)

Purity: >98 % , as determined by Coomassie stained SDS-PAGE and HPLC analysis.

Product Details

Protein Characteristics: AA 70-244, N-Term

Endotoxin Level:

Less than 0.1 ng per μg of protein.

Application Details

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

Comment:

Biological activity: The expected ED50 is 10.0 - 25.0 ng/ml, corresponding to a specific activity of 0.4 - 1.0 x 105 units/mg as determined by its ability to induce NF-κB in RAW264.7 cells in the absence of any cross-linking.

Restrictions: For Research Use only

Handling

Format: Lyophilized

Reconstitution: For maximum results, quick spin vial prior to opening. Reconstitute in water to a concentration of 0.1-1.0 mg/mL. Do not vortex. It is recommended to further dilute in a buffer, such as 5 % Trehalose, and store working aliquots at -20 °C to -80 °C.

Buffer: Lyophilized, carrier-free.

Handling Advice: Avoid repeated freeze/thaw cycles.

Storage: -20 °C

Storage Comment: Unopened vial can be stored at -20°C or -70°C.

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 (MMP-14) and ADAM10. Suppression of MMP-14 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 176 amino acid N-terminal methionylated recombinant protein has a predicted molecular mass of 20 kDa. The predicted N-terminal amino acid is Met.

Pathways: NF-kappaB Signaling