Granzyme B Mouse anti-Human, Clone: GrB-7, Invitrogen
Mouse Monoclonal Antibody
Manufacturer: Invitrogen MA135461
This antibody cannot be used on frozen sections in IHC applications.Granzyme B is a member of the granzyme serine protease family, and is found in the granules of cytotoxic T cells and NK cells. Granzyme B has been described as CGL1 (cathepsin G-like-1), a serine protease expressed only in cytotoxic T-lymphocytes after cell activation, and CTLA-1 (cytotoxic T lymphocyte-associated serine esterase 1) based on identification of mRNA in various cytotoxic T cells, but not observed in non-cytotoxic lymphoid cells. Granzyme B is crucial for the rapid induction of target cell death by apoptosis, induced by interaction with cytotoxic T cells. The receptor involved in this process has been identified as mannose 6-phosphate receptor which functions as a death receptor for Granzyme B during cytotoxic T cell-induced apoptosis. Granzyme B enters target cells to cleave caspase-3 and initiate the caspase cascade leading to DNA fragmentation and apoptosis. Granzyme B can also act through a mitochondrial apoptosis pathway by cleaving the Bid protein. Granzymes are neutral serine proteases, which are stored in specialized lytic granules of cytotoxic T lymphocytes (CTLs) and in natural killer (NK) cells. A number of granzymes (A to G) have been isolated and cloned from mouse CTLs and NK cells, however in man, fewer have been cloned and identified.
|Recombit human granzyme B.|
|Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.|
|Immunohistochemistry (Paraffin), Western Blot|
|tissue culture supernatant with 1% BSA and 0.09% sodium azide|
|CCPI, CGL-1, CGL1, CSP-B, CSPB, CTLA1, CTSGL1, HLP, SECT|
We continue to work to improve your shopping experience and your feedback regarding this content is very important to us. Please use the form below to provide feedback related to the content on this product.
Your feedback has been submitted. Fisher Scientific is always working to improve our content for you. We appreciate your feedback.Ok