Human MHC Class I Polypeptide-related Sequence B, MICB ELISA Kit (DEIA266)

Regulatory status: For research use only, not for use in diagnostic procedures.

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5 plates
Species Reactivity
Intended Use
The human MICB ELISA kit is for the quantitative determination of human MICB.
Contents of Kit
1. Capture Antibody: 0.5 mg/mL of mouse anti-MICB monoclonal antibody. Dilute to a working concentration of 0.5μg/mL in CBS before coating.
2. Detection Antibody: Each vial contains70μgbiotinylated rabbit anti-MICB polyclonal antibody. Reconstitute with 1 mL Detection antibody dilution buffer. After reconstitution, store at -20°C to-70°C in a manual defrost freezer. Dilute to a working concentration of 0.5μg/mL in Detection antibody dilution buffer before use.
3. Standard: Each vial contains 50ng of recombinant MICB. Reconstitute with 1 mL Detection antibody dilution buffer.
4. Streptavidin-HRP: 50 μL of streptavidin conjugated to horse-radish-peroxidase. 1:2,000 Dilution in Detection antibody dilution buffer before use.
Store the unopened kit at 4°C upon receipt and when it is not in use. For more detailed information, please download the following document on our website.
Detection Limit
39.1 pg/mL


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A role for the MHC class I-like Mill molecules in nutrient metabolism and wound healing


Authors: Rabinovich, Brian A.; Ketchem, Randal R.; Wolfson, Martin; Goldstein, Lynn; Skelly, Marylin; Cosman, David

MHC class I family members serve multiple functions beyond antigen presentation. We provide insight into the structure, expression and function of the Mill subfamily. This family includes two surface glycoproteins, Mill1 and Mill2. Protein sequences for Mill1 and Mill2 are most highly related to the NKG2D ligands, MICA and MICB, but neither of them bound to NKG2D. Computer-based protein modelling indicated that hereditary haemochromatosis protein (HFE), a molecule involved in iron uptake, was most similar. Mill1 and Mill2 were observed on cycling thymocytes, proliferating smooth muscle cells and fibroblasts. Using soluble Mill proteins, we found evidence for a soluble ligand in serum. Like HFE, the Mill family may be involved in nutrient metabolism. Skin was one of the only three organs found to express transcripts for both Mill1 and Mill2. Addition of antibodies specific for Mill2 to wounded skin enhanced healing. Our results suggest a role for the Mill proteins in cellular metabolism, with possible therapeutic significance.

A compendium of adenovirus genetic modifications for enhanced replication, oncolysis, and tumor immunosurveillance in cancer therapy


Authors: Stepanenko, Aleksei A.; Chekhonin, Vladimir P.

In this review, we specifically focus on genetic modifications of oncolytic adenovirus 5 (Ad5)-based vectors that enhance replication, oncolysis/spread, and virus-mediated tumor immunosurveillance. The finding of negative regulation of minor core protein V by SUMOylation led to the identification of amino acid residues, which when mutated increase adenovirus replication and progeny yield. Suppression of Dicer and/or RNAi pathway with shRNA or p19 tomato bushy stunt protein also results in significant enhancement of adenovirus replication and progeny yield. Truncation mutations in E3-19K or i-leader sequence or overexpression of adenovirus death protein (ADP) potently increase adenovirus progeny release and spread without affecting virus yield. Moreover, E3-19K protein, which was found to inhibit both major histocompatibility complex I (MHCI) and MHC-I chain related A and B proteins (MICA/MICB) expression on the cell surface, protecting infected cells from T-lymphocyte and natural killer (NK) cell attack, may be tailored to selectively target only MHCI or MICA/MICB, or to lose the ability to downregulate both. At last, E3-19K protein may be exploited to deliver tumor-associated epitopes directly to the endoplasmic reticulum for loading MHCI in the transporter associated with antigen processing (TAP)-deregulated cells.

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