Monoclonal Anti-B2M Antibody, Mouse IgG2b (BBM.1)

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B2M-M614c-25tests
$60.00
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B2M-M614c-200tests
$330.00
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Source

Monoclonal Anti-B2M Antibody, Mouse IgG2b (BBM.1) is a mouse monoclonal antibody recombinantly expressed from human 293 cells (HEK293), which provides higher batch consistency and long term security of supply.

Antibody Type

Recombinant Monoclonal

Clone

BBM.1

Isotype

Mouse IgG2b, Kappa

Host Species

Mouse

Reactivity

Human

Immunogen

MOLT-4, a Human acute lymphoblastic leukemia cell line

Specificity

Clone BBM.1 detects Beta-2-microglobulin in human.

Application

ELISA (Evaluation of levels of B2M protein).

Flow Cytometry (Evaluation of an epitope within the extracellular domain of human B2M protein).

Recommended Dilution

1:50

Isotype Control

The isotype control is sold separately; please refer to Cat. No. DNP-M486 for product information.

Form

Lyophilized

Formulation

Lyophilized from a 0.22 μm-filtered solution in PBS (pH 7.4), with trehalose as protectant.

Please contact us for customized product forms or formulations.

Reconstitution

Please refer to the Certificate of Analysis (CoA) for specific instructions.

Shipping

Lyophilized product is shipped at ambient temperature.

Storage

For long term storage, the product should be stored in a lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:
  • -20°C to -70°C for 24 months in lyophilized state;
  • -70°C for 12 months after reconstitution.
  • 2-8 °C for 12 months after reconstitution.
Notices

Product Specific Notices: For research use only.

Background

Beta-2-microglobulin (B2M) is a component of the class I major histocompatibility complex (MHC) and involved in the presentation of peptide antigens to the immune system. B2M consists of two β sheets joined by a disulfide bond, which could form amyloid fibrils in some pathological conditions. Increasing evidence has indicated that B2M gene alterations in tumor cells may lower the efficacy of T-cell based immunotherapies by hampering MHC class I-mediated tumor antigen presentation and avoiding T cell recognition.