Recombinant human RANKL protein - Bioactive cytokine

Recombinant cytokine, source: E. coli

SPECIFICATIONS

Specifications

Source
E. coli
Species
Human
Synonyms
TNFSF11
Tumor necrosis factor ligand superfamily member 11
TNF-related activation-induced cytokine
TRANCE
Accession sequence

O14788

Molecular weight
~ 20 kDa (SDS-PAGE)
Carrier
Carrier-free
Tag
Tag-free
Purity
≥95% (SDS-PAGE)
Solubility

100 μg/ml in water

Formulation buffer

Solution containing Tris-HCl and NaCl

Appearance (form)
Lyophilized
Reconstitution buffer
1X PBS with 0.1 % BSA or HSA (not provided)
Endotoxin

The absence of bacterial contamination (e.g. lipoproteins and endotoxins) has been confirmed using HEK-Blue™ TLR2 and HEK‑Blue™ TLR4 cells.

Tested applications

Cellular assays

Quality control

Each lot is functionally tested and validated.

CONTENTS

Contents

  • Product: 
    Recombinant human RANKL
  • Cat code: 
    rcyec-hrankl
  • Quantity: 
    10 µg

Shipping & Storage

  • Shipping method:  Room temperature
  • Storage:

    • -20°C

    Caution:

    • Avoid repeated freeze-thaw cycles

Details

RANKL background

Receptor Activator of NF-κB Ligand (RANKL), also known as member 11 of the tumor necrosis factor (TNF) superfamily (TNFSF11) or TNF-related activation-induced cytokine (TRANCE), exists as a transmembrane or soluble protein produced by osteoblasts and activated T cells [1]. RANKL binds to its receptor RANK via an obligate trimer configuration [1, 2]. RANKL/RANK signaling plays a pivotal role in bone remodeling and dendritic cell survival, thereby enhancing the induction of T cell responses [1]. Upon RANKL binding, RANK trimers recruit TNF receptor-associated factor (TRAF) adaptor proteins, such as TRAF6, to TRAF-binding motifs within their cytoplasmic domains [1]. The TRAF6 signaling cascade results in the activation of NF-κB and AP-1 transcription factors. Multiple efforts have focused on the development of anti‑RANKL antibodies or small‑molecule inhibitors for blocking RANKL/RANK signaling to reduce osteoporosis, prevent skeletal-related events (SREs) from bone metastasis in cancer, or improve anti-tumor immunity [1-3].

 

1. Cheng ML. & Fong L., 2014. Effects of RANKL-targeted therapy in immunity and cancer. Front. Oncol. 3:329.
2. Ahern E. et al., 2018. Roles of the RANKL-RANK axis in anti-tumour immunity — implications for therapy. Nat. Rev. Clin. Oncol. 15:676-93.
3. Nakai Y. et al., 2019. Efficacy of an orally active small-molecule inhibitor of RANKL in bone metastasis. Bone Res. 7:1.

CUSTOMER SERVICE & TECHNICAL SUPPORT

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