RANKL Antibody [K7M17] | Primary Antibodies

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000-1:2000 IHC1:400-1:2000 IF1:200

Application
WB, IHC, IF

Reactivity
Human

Source
Mouse Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
35 kDa 28 kDa, 35 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Positive Control	Human lymph node tissue; Human liver tissue; HeLa cells
Negative Control

Datasheet & SDS

Biological Description

Specificity
RANKL Antibody [K7M17] detects endogenous levels of total RANKL protein.

Clone
K7M17

Synonym(s)
CD254; OPGL; RANKL; TRANCE; TNFSF11; Tumor necrosis factor ligand superfamily member 11; TNF-related activation-induced cytokine; ODF; RANKL; TRANCE

Background
RANKL, or Receptor Activator of Nuclear factor Kappa-B Ligand (also known as TRANCE or OPGL), is a type II transmembrane protein belonging to the TNF superfamily, consisting of 314 amino acids in humans and encoded by the TNFSF11 gene. It is produced by osteoblasts, T cells, mammary epithelial cells, and endothelial cells, and exists in both membrane-bound and soluble forms due to proteolytic cleavage by enzymes such as TACE, ADAM10, and MMPs, or through alternative splicing. The receptor-binding ectodomain of RANKL self-assembles into a stable homotrimer with a jellyroll beta-sandwich fold, comprising ten hydrogen-bonded beta-strands in two sheets and featuring three equivalent receptor-binding clefts lined by unique AA′′, CD, DE, and EF loops, which impart specificity for its receptor RANK over the decoy receptor OPG. These critical residues within these loops are necessary for receptor activation. RANKL plays a central role in osteoclastogenesis by binding to RANK on osteoclast precursors, forming signaling complexes in a 3:3 stoichiometry that activate TRAFs and FADD, subsequently triggering NF-kappaB, MAPK (JNK, p38, ERK), and calcium oscillations to induce osteoclast differentiation, fusion, activation, and survival, thus regulating bone resorption and calcium homeostasis. RANKL is essential for lymphoid organogenesis, dendritic cell survival, mammary gland development and lactation, thymic medullary epithelial cell expansion, and broader immune cell interactions, with OPG serving as an antagonist to modulate signaling intensity. RANKL is implicated in osteoporosis, where an increased RANKL to OPG ratio enhances bone resorption, as well as in rheumatoid arthritis with synovial inflammation, bone metastases leading to tumor-induced osteolysis, and rare cases of osteopetrosis, where RANKL deficiency results in abnormally high bone density and lymphoid developmental defects.

Background

RANKL, or Receptor Activator of Nuclear factor Kappa-B Ligand (also known as TRANCE or OPGL), is a type II transmembrane protein belonging to the TNF superfamily, consisting of 314 amino acids in humans and encoded by the TNFSF11 gene. It is produced by osteoblasts, T cells, mammary epithelial cells, and endothelial cells, and exists in both membrane-bound and soluble forms due to proteolytic cleavage by enzymes such as TACE, ADAM10, and MMPs, or through alternative splicing. The receptor-binding ectodomain of RANKL self-assembles into a stable homotrimer with a jellyroll beta-sandwich fold, comprising ten hydrogen-bonded beta-strands in two sheets and featuring three equivalent receptor-binding clefts lined by unique AA′′, CD, DE, and EF loops, which impart specificity for its receptor RANK over the decoy receptor OPG. These critical residues within these loops are necessary for receptor activation. RANKL plays a central role in osteoclastogenesis by binding to RANK on osteoclast precursors, forming signaling complexes in a 3:3 stoichiometry that activate TRAFs and FADD, subsequently triggering NF-kappaB, MAPK (JNK, p38, ERK), and calcium oscillations to induce osteoclast differentiation, fusion, activation, and survival, thus regulating bone resorption and calcium homeostasis. RANKL is essential for lymphoid organogenesis, dendritic cell survival, mammary gland development and lactation, thymic medullary epithelial cell expansion, and broader immune cell interactions, with OPG serving as an antagonist to modulate signaling intensity. RANKL is implicated in osteoporosis, where an increased RANKL to OPG ratio enhances bone resorption, as well as in rheumatoid arthritis with synovial inflammation, bone metastases leading to tumor-induced osteolysis, and rare cases of osteopetrosis, where RANKL deficiency results in abnormally high bone density and lymphoid developmental defects.

References
https://pubmed.ncbi.nlm.nih.gov/32047573/ https://pubmed.ncbi.nlm.nih.gov/35181574/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%