InVivoMAb anti-mouse Kappa Immunoglobulin Light Chain

Catalog #BE0176
Clone:
187.1 (HB-58)
Reactivities:
Mouse

$164.00 - $4,280.00

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  • 100 mg - $4,280.00
  • 50 mg - $3,024.00
  • 25 mg - $2,009.00
  • 5 mg - $600.00
  • 1 mg - $164.00
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Product Details

The 187.1 monoclonal antibody reacts with the kappa chain of the mouse immunoglobulin light chain. The κ chain is one of two types of polypeptide subunits which make up the immunoglobulin light chain. A typical antibody is composed of two immunoglobulin heavy chains and two immunoglobulin light chains. The κ chain is coded for by V (variable), J (joining) and C (constant) genes. These genes undergo V(D)J recombination to generate a diverse repertoire of immunoglobulins.

Specifications

Isotype Rat IgG1, κ
Recommended Isotype Control(s) InVivoMAb rat IgG1 isotype control, anti-horseradish peroxidase
Recommended Dilution Buffer InVivoPure pH 7.0 Dilution Buffer
Conjugation This product is unconjugated. Conjugation is available via our Antibody Conjugation Services.
Immunogen Mouse IgG2b Isotype control antibody clone MPC-11
Reported Applications Immunofluorescence
Formulation PBS, pH 7.0
Contains no stabilizers or preservatives
Endotoxin <2EU/mg (<0.002EU/μg)
Determined by LAL gel clotting assay
Purity >95%
Determined by SDS-PAGE
Sterility 0.2 µm filtration
Production Purified from cell culture supernatant in an animal-free facility
Purification Protein G
RRID AB_10948999
Molecular Weight 150 kDa
Storage The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.
Immunofluorescence
Burbage, M., et al. (2015). "Cdc42 is a key regulator of B cell differentiation and is required for antiviral humoral immunity" J Exp Med 212(1): 53-72. PubMed

The small Rho GTPase Cdc42, known to interact with Wiskott-Aldrich syndrome (WAS) protein, is an important regulator of actin remodeling. Here, we show that genetic ablation of Cdc42 exclusively in the B cell lineage is sufficient to render mice unable to mount antibody responses. Indeed Cdc42-deficient mice are incapable of forming germinal centers or generating plasma B cells upon either viral infection or immunization. Such severe immune deficiency is caused by multiple and profound B cell abnormalities, including early blocks during B cell development; impaired antigen-driven BCR signaling and actin remodeling; defective antigen presentation and in vivo interaction with T cells; and a severe B cell-intrinsic block in plasma cell differentiation. Thus, our study presents a new perspective on Cdc42 as key regulator of B cell physiology.