Granzyme A Set Mouse anti-Human, FITC, Clone: CB9, BD

Description

• The primary mechanism by which cytotoxic T cells eliminate virally infected cells is by granule exocytosis
• The release of cytotoxic granule contents by cytotoxic T lymphocytes (CTL) triggers apoptotic target cell death
• CTL granules contain a pore-forming protein, perforin, and a group of serine proteases called granzymes
• In the classic model, perforins create holes in the target cell membrane, allowing entrance of the granzymes
• Granzyme A and B are the predominant granzymes activated after CTL activation, but each act via an independent apoptotic pathway; granzyme B is activated immediately, while granzyme A acts hours later
• Granzyme B does not induce cleavage of caspase-3, lamin B, rho-GTPase or PARP, but does cleave DNA-PKcs and nuclear mitotic apparatus protein (NuMA)
• The physiological substrates for granzyme A in the apoptotic pathway have not been identified
• Studies involving mice which are deficient in both granzyme A and B suggest a model whereby the granzyme B pathway may have evolved as the major apoptotic pathway with the granzyme A pathway acting as a backup
• However, further research is needed to delineate the components of the distinct pathways
• Clone CB9 recognizes human granzyme A
• Purified human granzyme A was used as immunogen
• Clone MOPC-21 is a mouse IgG1 isotype (negative) control
• The MOPC-21 antibody has unknown specificity
• CB9 and MOPC-21 FITC conjugates are optimized in F/P ratios
• The antibodies are routinely tested in parallel by flow cytometry
• Other applications were tested at BD Biosciences Pharmingen during antibody development only or reported in the literature.