B2M Antibody
Mouse Monoclonal Antibody (Mab)
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Application
| WB |
|---|---|
| Primary Accession | P61769 |
| Other Accession | NP_004039.1 |
| Reactivity | Mouse, Rat, Human |
| Host | Mouse |
| Clonality | Monoclonal |
| Calculated MW | 13715 Da |
| Isotype | IgG1 |
| Antigen Source | HUMAN |
| Gene ID | 567 |
|---|---|
| Antigen Region | 10-39 aa |
| Other Names | B2M; Beta-2-microglobulin; Beta-2-microglobulin form pI 5.3 |
| Dilution | WB~~1:1000 |
| Target/Specificity | This B2M antibody is generated from mice immunized with a KLH conjugated synthetic peptide between 10-39 amino acids from human B2M. |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | B2M Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | B2M (HGNC:914) |
|---|---|
| Function | Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system. Exogenously applied M.tuberculosis EsxA or EsxA-EsxB (or EsxA expressed in host) binds B2M and decreases its export to the cell surface (total protein levels do not change), probably leading to defects in class I antigen presentation (PubMed:25356553). |
| Cellular Location | Secreted. Cell surface. Note=Detected in serum and urine (PubMed:1336137, PubMed:7554280). {ECO:0000269|PubMed:7554280, ECO:0000269|Ref.6} |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
This gene encodes a serum protein found in association with the major histocompatibility complex (MHC) class I heavy chain on the surface of nearly all nucleated cells. The protein has a predominantly beta-pleated sheet structure that can form amyloid fibrils in some pathological conditions. A mutation in this gene has been shown to result in hypercatabolic hypoproteinemia.
REFERENCES
Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010)
Rennella, E., et al. J. Mol. Biol. 401(2):286-297(2010)
Debelouchina, G.T., et al. J. Am. Chem. Soc. 132(30):10414-10423(2010)
Mumtaz, A., et al. Saudi J Kidney Dis Transpl 21(4):701-706(2010)
Guo, H.C., et al. Nature 360(6402):364-366(1992)
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