ACROBiosystems社 プロダクトリスト：Recombinant Protein
- Human MS4A1 / CD20 Protein, Fc Tag
- 100ug: 87,000円
|Characteristics||This protein carries a human IgG1 Fc tag at the N-terminus. The protein has a calculated MW of 33.4 kDa. The protein migrates as 42 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.|
|Endotoxin Level||Less than 1.0 EU per μg by the LAL method.|
|Purity||>90% as determined by SDS-PAGE.|
|Description||B-lymphocyte antigen CD20 is also known as B-lymphocyte surface antigen B1, Leukocyte surface antigen Leu-16, Membrane-spanning 4-domains subfamily A member 1 and MS4A1, is an activated-glycosylated phosphoprotein expressed on the surface of all B-cells beginning at the pro-B phase (CD45R+, CD117+) and progressively increasing in concentration until maturity. CD20 is expressed on all stages of B cell development except the first and last; it is present from late pro-B cells through memory cells, but not on either early pro-B cells or plasma blasts and plasma cells. It is found on B-cell lymphomas, hairy cell leukemia, B-cell chronic lymphocytic leukemia, and melanoma cancer stem cells. The protein has no known natural ligand and its function is to enable optimal B-cell immune response, specifically against T-independent antigens. It is suspected that it acts as a calcium channel in the cell membrane. CD20 / MS4A1 is the target of the monoclonal antibodies (mAb) rituximab, Ibritumomab tiuxetan, and tositumomab, which are all active agents in the treatment of all B cell lymphomas and leukemias. Defects in CD20 / MS4A1 are the cause of immunodeficiency common variable type 5 (CVID5); also called antibody deficiency due to CD20 defect. CVID5 is a primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen.|
|Reference||(1) Walport M, et al., 2008, Janeway's Immunobiology (7th ed.). New York: Garland Science.
(2) Bonilla FA, Bona CA., 1996, Textbook of Immunology. Boca Raton: CRC. p. 102.
(3) Cragg MS., 2005., Curr. Dir. Autoimmun. 8: 140?74.