Validation Data Gallery
|Positive WB detected in
|mouse kidney tissue, HEK-293 cells, HeLa cells, HepG2 cells, human heart tissue, human liver tissue, MCF-7 cells, mouse pancreas tissue
|Positive IP detected in
|Positive IHC detected in
|human pancreas cancer tissue
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Western Blot (WB)
|WB : 1:500-1:2000
|IP : 0.5-4.0 ug for 1.0-3.0 mg of total protein lysate
|IHC : 1:20-1:200
|It is recommended that this reagent should be titrated in each testing system to obtain optimal results.
|Sample-dependent, check data in validation data gallery
14613-1-AP targets RBPJ in WB, IP, IHC, ELISA applications and shows reactivity with human, mouse samples.
|Host / Isotype
|Rabbit / IgG
|RBPJ fusion protein Ag6206
|recombination signal binding protein for immunoglobulin kappa J region
|Calculated molecular weight
|Observed molecular weight
|GenBank accession number
|Gene ID (NCBI)
|Antigen affinity purification
|PBS with 0.02% sodium azide and 50% glycerol pH 7.3.
|Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage. 20ul sizes contain 0.1% BSA.
RBPJ, also named as IGKJRB, IGKJRB1, RBPJK, RBPSUH, NY-REN-30, CBF-1 and CSL, belongs to the Su(H) family. It is a transcriptional regulator that plays a central role in Notch signaling, a signaling pathway involved in cell-cell communication that regulates a broad spectrum of cell-fate determinations. RBPJ acts as a transcriptional repressor when it is not associated with Notch proteins. It is specifically binds to the immunoglobulin kappa-type J segment recombination signal sequence. RBPJ binds to the Runx3 promoter in the atrioventricular canal in vivo, and inhibition of Notch reduces RUNX3 expression in the cardiac cushion of embryonic hearts.
Blockade of the Arid5a/IL-6/STAT3 axis underlies the anti-inflammatory effect of Rbpjl in acute pancreatitis.
J Biol Chem
RUNX3 maintains the mesenchymal phenotype after termination of the Notch signal.
DAPT Attenuates Cadmium-Induced Toxicity in Mice by Inhibiting Inflammation and the Notch/HES-1 Signaling Axis.
Salidroside alleviates cadmium-induced toxicity in mice by restoring the notch/HES-1 and RIP1-driven inflammatory signaling axis.
Gisenoside Rg1 attenuates cadmium-induced neurotoxicity in vitro and in vivo by attenuating oxidative stress and inflammation
Edaravone attenuates cadmium-induced toxicity by inhibiting oxidative stress and inflammation in ICR mice.