InVivoMAb anti-mouse Kappa Immunoglobulin Light Chain

Clone Catalog # Category
187.1 (HB58) BE0176 InVivoMab Antibodies
$95 - $3250

About InVivoMAb anti-mouse Kappa Immunoglobulin Light Chain

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.

InVivoMAb anti-mouse Kappa Immunoglobulin Light Chain Specifications

Isotype

Rat IgG1, κ

Recommended Isotype Control(s) InVivoMAb rat IgG1 isotype control, anti-horseradish peroxidase(BE0088)
Recommended InVivoPure Dilution Buffer InVivoPure pH 7.0 Dilution Buffer(IP0070)
Immunogen

Mouse IgG2b Isotype control antibody clone MPC-11

Reported Applications

Immunofluorescence

Endotoxin
  • <2EU/mg (<0.002EU/μg)
  • Determined by LAL gel clotting assay
Purity
  • >95%
  • Determined by SDS-PAGE
Formulation
  • PBS, pH 7.0
  • Contains no stabilizers or preservatives
Sterility

0.2 μM filtered

Production

Purified from tissue culture supernatant in an animal free facility

Purification

Protein G

Storage

The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.

RRID

AB_10948999

Molecular Weight

150 kDa

Application References

InVivoMAb anti-mouse Kappa Immunoglobulin Light Chain (Clone: 187.1 (HB58))

  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.

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