Gasdermin Family Antibody Sampler Kit #26776
Product Information
Kit Usage Information
Protocols
- 7074: Western Blotting
- 19453: Western Blotting, Immunofluorescence*
- 36425: Western Blotting, Immunoprecipitation (Agarose), Immunohistochemistry (Paraffin)
- 49307: Western Blotting, Immunoprecipitation (Agarose)
- 55879: Western Blotting, Immunofluorescence*
- 69469: Western Blotting, Immunoprecipitation (Agarose), Immunofluorescence*
- 76439: Western Blotting, Immunoprecipitation (Agarose)
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).
Like other gasdermin family members, Gasdermin E (also called DFNA5) contains an amino-terminal pore forming domain that triggers pyroptosis. Cleavage of Gasdermin E at Asp270 is induced by apoptotic-associated caspase-3, converting apoptotic signals to pyroptosis (8). In addition, cleavage of Gasdermin E can be induced by Granzyme B secreted by NK cells and contributes to tumor suppressive activity (9). Gasdermin E expression is suppressed in several types of cancer, including gastric, colorectal, and breast carcinoma, and may be associated with decreased survival (10-12). In contrast, an increase in Gasdermin E, including the amino-terminal pore-forming fragment, is associated with conditions of excessive inflammation (13-15). Gasdermin A (GSDMA) is preferentially expressed in the epithelium of the skin and gastrointestinal tract and is frequently suppressed in gastric cancer (16-18). Gasdermin B (GSDMB) has been reported to be upregulated in several tumor types, and in breast cancer has been associated with metastasis and poor prognosis (19,20). In addition, Gasdermin B has been associated with immune disorders, including asthma (21,22). Gasdermin B can be cleaved by Granzyme A secreted from cytotoxic lymphocytes leading to pyroptotic cell death (23).
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- Rogers, C. et al. (2017) Nat Commun 8, 14128.
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- Yokomizo, K. et al. (2012) Anticancer Res 32, 1319-22.
- Tan, G. et al. (2021) Cell Rep 35, 109265.
- Li, Y. et al. (2021) Cell Death Differ 28, 2333-2350.
- Shi, H. et al. (2021) Circ Res 129, 383-396.
- Tamura, M. et al. (2007) Genomics 89, 618-29.
- Saeki, N. et al. (2000) Mamm Genome 11, 718-24.
- Saeki, N. et al. (2007) Oncogene 26, 6488-98.
- Hergueta-Redondo, M. et al. (2014) PLoS One 9, e90099.
- Hergueta-Redondo, M. et al. (2016) Oncotarget 7, 56295-56308.
- Yu, J. et al. (2011) Pediatr Pulmonol 46, 701-8.
- Das, S. et al. (2016) Proc Natl Acad Sci USA 113, 13132-13137.
- Zhou, Z. et al. (2020) Science 368, eaaz7548. doi: 10.1126/science.aaz7548.
Limited Uses
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