Gasdermin C (F9R3M) Rabbit mAb #61921
- WB
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 59 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Protocol
Specificity / Sensitivity
Gasdermin C (F9R3M) Rabbit mAb recognizes endogenous levels of total Gasdermin C protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro125 of human Gasdermin C protein.
Background
The gasdermin family, which includes GSDMA, GSDMB, GSDMC, GSDMD, and GSDME, has been shown to play a role in inflammation and cell death. Gasdermin D has been reported to have a critical role as a downstream effector of pyroptosis (1,2). Pyroptosis is a lytic type of cell death triggered by inflammasomes, multiprotein complexes assembled in response to pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs) that result in the activation of caspase-1 and subsequent cleavage of pro-inflammatory cytokines IL-1β and IL-18 (3). Gasdermin D was identified by two independent groups as a substrate of inflammatory caspases, caspase-1 and caspase-11/4/5, producing two fragments: GSDMD-N and GSDMD-C. Cleavage results in release of an intramolecular inhibitory interaction between the N- and C-terminal domains, allowing the N-terminal fragment GSDMD-N to initiate pyroptosis through the formation of pores on the plasma membrane (4-7).
Overexpression of Gasdermin C (GSDMC) in several types of cancer has been associated with disease progression and prognosis (8-13). Cleavage of GSDMC can be induced by caspase-8, with the N-terminal fragment initiating pyroptosis (14,15).
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- Hou, J. et al. (2020) Nat Cell Biol 22, 1264-1275.
- Zhang, J.Y. et al. (2021) Cell Res 31, 980-997.
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