CD59 / Complement Regulatory Protein / Protectin Antibody - Without BSA and Azide
Mouse Monoclonal Antibody [Clone MACIF/1193 ]
|Application ||IHC, IF, FC|
|Other Accession||966, 278573, 709466, 710641|
|Isotype||Mouse / IgM, kappa|
|Other Names||CD59 glycoprotein, 1F5 antigen, 20 kDa homologous restriction factor, HRF-20, HRF20, MAC-inhibitory protein, MAC-IP, MEM43 antigen, Membrane attack complex inhibition factor, MACIF, Membrane inhibitor of reactive lysis, MIRL, Protectin, CD59, CD59, MIC11, MIN1, MIN2, MIN3, MSK21|
|Storage||Store at 2 to 8°C.Antibody is stable for 24 months.|
|Precautions||CD59 / Complement Regulatory Protein / Protectin Antibody - Without BSA and Azide is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||MIC11, MIN1, MIN2, MIN3, MSK21|
|Function||Potent inhibitor of the complement membrane attack complex (MAC) action. Acts by binding to the C8 and/or C9 complements of the assembling MAC, thereby preventing incorporation of the multiple copies of C9 required for complete formation of the osmolytic pore. This inhibitor appears to be species-specific. Involved in signal transduction for T-cell activation complexed to a protein tyrosine kinase.|
|Cellular Location||Cell membrane; Lipid-anchor, GPI-anchor. Secreted. Note=Soluble form found in a number of tissues|
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Provided below are standard protocols that you may find useful for product applications.
Reacts with human CD59, a 20kDa glycosyl phosphatidyl-inositol (GPI)-anchored cell surface protein. CD59 regulates complement-mediated cell lysis, and it is involved in lymphocyte signal transduction. This protein is a potent inhibitor of the complement membrane attack complex, whereby it binds complement C8 and/or C9 during the assembly of this complex, thereby inhibiting the incorporation of multiple copies of C9 into the complex, which is necessary for osmolytic pore formation. CD59 is widely distributed on cells in all tissues. It inhibits formation of MAC, thus protecting cells from complement-mediated lysis. The expression of CD59 on erythrocytes is important for their survival. Genetic defects in GPI-anchor attachment, that cause a reduction or loss of CD59 and CD55 on erythrocytes produce the symptoms of the disease paroxysmal hemoglobinuria (PNH). It is useful for study on GPI-anchored proteins, PNH and CD59 functions.
A E Fritzinger, F. Marciano-Cabral, et al. (2006) Infection and Immunity 74(2):1189-1195. | J Zhang, C Gerhardinger, M Lorenzi (2002) Diabetes 51(12): 3499-3504 |
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