anti-Gasdermin D (mouse), pAb (IN110)
Method: Gasdermin D is analyzed by Western blot in cell extracts of bone marrow-derived macrophage cells (BMDMs) (WT, Gasdermin -/- or Asc -/-) treated with LPS (50ng/ml) for 3h and +/- Nigericin (5μM for 2.5h, Prod. No. AG-CN2-0020). Cell extracts are separated by SDS-PAGE under reducing conditions, transferred to nitrocellulose and incubated with anti-Gasdermin D (mouse), pAb (IN110) (0.5µg/ml). After addition of an anti-Guinea Pig secondary antibody coupled to HRP (1/5000), proteins are visualized by a chemiluminescence detection system.
Picture courtesy of Prof. Olaf Gross, University Medical Center Freiburg, Germany
|Synonyms||Gasdermin Domain-containing Protein 1; Gasdermin-D (C-terminal); GSDMD-CT; Gsdmd|
|Product Type||Polyclonal Antibody|
|Immunogen/Antigen||Recombinant mouse gasdermin D (C-terminus).|
Western Blot: (1:2'000)*
*Note: We recommend a starting dilution of 1:2'000 and to optimize the dilution depending on your cells/tissues.
Recognizes full-length and cleaved C-terminus domain of mouse gasdermin D. Does not cross-react with human gasdermin D.
|Purity Detail||Protein A affinity purified.|
|Formulation||Liquid. In PBS containing 10% glycerol and 0.02% sodium azide.|
|Other Product Data||
UniProt link Q9D8T2: Gasdermin D (mouse)
|Shipping and Handling|
|Short Term Storage||+4°C|
|Long Term Storage||-20°C|
After opening, prepare aliquots and store at -20°C.
Avoid freeze/thaw cycles.
|Use/Stability||Stable for at least 1 year after receipt when stored at -20°C.|
|Product Specification Sheet|
Inflammasomes are multimeric protein complexes that comprise a sensor (e.g. NLRP3), an adaptor (ASC/Pycard) and the procaspase-1. An inflammasome assembles in response to a diverse range of pathogen-associated or danger-associated molecular patterns (PAMPs or DAMPs). The inflammasome platform leads to activation of caspase-1, which further induces maturation of interleukin-1β and -18 (IL-1β and IL-18) through proteolytic cleavage of pro-IL-1β and pro-IL-18. Activated caspase-1, and also the recently characterized caspase-11 non-canonical inflammasome pathway, also cleave the intracellular gasdermin D, which leads to a particular form of inflammatory cell death called pyroptosis. The gasdermin family members contain N-terminal domains that are capable of forming membrane pores to induce cytolysis, whereas the C-terminal domains of gasdermins function as inhibitors of such cytolysis through intramolecular domain association. Caspase-1 or -11 cleavage of gasdermin D is required for regulation of pyroptosis: upon protease cleavage of the gasdermin N- and C-domain linker, the disruption of the intramolecular domain interaction in the presence of lipids releases the N-domain to assemble oligomeric membrane pores that trigger cell death. Gasdermin D seems to be a key effector in the LPS-induced lethal sepsis.
- RNA viruses promote activation of the NLRP3 inflammasome through cytopathogenic effect-induced potassium efflux: L. Silva da Costa, et al.; Cell Death Dis. 10, 346 (2019)
- IKKβ is required for the formation of the NLRP3 inflammasome: S.K. Nanda, et al.; EMBO Rep. e50743 (2021)
- GSK3β mediates the spatiotemporal dynamics of NLRP3 inflammasome activation: S. Arumugam, et al.; Cell Death Differ. ahead of print (2022)
- dsDNA-induced AIM2 pyroptosis halts aberrant inflammation during rhabdomyolysis-induced acute kidney injury: C. Baatarjav, et al.; Cell Death Differ. ahead of print (2022)