Cet anticorps anti-BCL10 Polyclonal Lapin (ABIN7225718) détecte spécifiquement BCL10 dans WB, IHC, ELISA et IF.
L’anticorps est réactif avec des échantillons de Humain, Souris et Rat.
BCL10
Reactivité: Humain, Souris, Rat
WB, IHC, IHC (p)
Hôte: Lapin
Polyclonal
unconjugated
Indications d'application
Optimal working dilutions should be determined experimentally by the investigator. Suggested starting dilutions are as follows: WB 1:500-1:2000,IHC 1:100-1:300,ELISA 1:40000,IF 1:50-200
Restrictions
For Research Use only
Format
Liquid
Concentration
1 mg/mL
Buffer
Liquid in PBS containing 50 % glycerol, 0.5 % BSA and 0.02 % sodium azide.
Agent conservateur
Sodium azide
Précaution d'utilisation
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Stock
-20 °C
Stockage commentaire
Stable for one year at -20°C from date of shipment. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap. Aliquot to avoid repeated freezing and thawing.
Date de péremption
12 months
Antigène
BCL10
(B-Cell CLL/lymphoma 10 (BCL10))
Autre désignation
Bcl-10
Sujet
BCL10, CIPER, CLAP, B-cell lymphoma/leukemia 10, B-cell CLL/lymphoma 10, Bcl-10, CARD-containing molecule enhancing NF-kappa-B, CARD-like apoptotic protein, hCLAP, CED-3/ICH-1 prodomain homologous E10-like regulator, CIPER, Cellular homologBCL10 (B-cell CLL/lymphoma 10) was identified by its translocation in a case of mucosa-associated lymphoid tissue (MALT) lymphoma. The protein encoded by BCL10 contains a caspase recruitment domain (CARD), and has been shown to induce apoptosis and to activate NF-kappaB. This protein is reported to interact with other CARD domain containing proteins including CARD9, 10, 11 and 14, which are thought to function as upstream regulators in NF-kappaB signaling. This protein is found to form a complex with MALT1, a protein encoded by another gene known to be translocated in MALT lymphoma. MALT1 and this protein are thought to synergize in the activation of NF-kappaB, and the deregulation of either of them may contribute to the same pathogenetic process that leads to the malignancy. Alternative splicing results in multiple transcript variants.