Granzyme C (E5M3N) Rabbit mAb #83424
- WB
- IF
Supporting Data
| REACTIVITY | M |
| SENSITIVITY | Endogenous |
| MW (kDa) | 25 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- M-Mouse
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunofluorescence (Frozen) | 1:800 - 1:1600 |
Storage
For a carrier free (BSA and azide free) version of this product see product #10352.
Protocol
Specificity / Sensitivity
Granzyme C (E5M3N) Rabbit mAb recognizes endogenous levels of total Granzyme C protein. This antibody does not cross-react with other Granzyme proteins.
Species Reactivity:
Mouse
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val190 of mouse Granzyme C protein.
Background
Granzymes are a family of serine proteases expressed by cytotoxic T lymphocytes and natural killer (NK) cells and are key components of immune responses to pathogens and transformed cells (1). In mice, ten family members have been identified: A, B, C, D, E, F, G, K, M, and N (2). Granzymes are synthesized as zymogens and are processed into mature enzymes by cleavage of a leader sequence. They are released by exocytosis in lysosome-like granules containing perforin, a membrane pore-forming protein (3). Granzyme C is the closest murine homolog of human Granzyme H and is located directly downstream of GzmB (4). Granzyme C has been demonstrated to induce cell death with a similar potency as Granzyme B, and CTLs from mice with reduced expression of Granzyme C and F display diminished cytotoxicity (5). Granzyme C has been identified as a marker for type 1 innate lymphoid cells (ILC1s) exhibiting cytotoxic effector function in addition to ‘helper-like’ function (6). These cells have been shown to regulate antitumor immunity and autoimmunity in mouse models (6).
- Trapani, J.A. (2001) Genome Biol 2, REVIEWS3014.
- Russell, J.H. and Ley, T.J. (2002) Annu Rev Immunol 20, 323-70.
- Lord, S.J. et al. (2003) Immunol Rev 193, 31-8.
- Cai, S.F. et al. (2009) J Immunol 182, 6287-97.
- Getachew, Y. et al. (2008) J Immunol 181, 7810-7.
- Nixon, B.G. et al. (2022) Sci Immunol 7, eabi8642.
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