Nano-SiO2
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Cat.code:
tlrl-sio-2
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ABOUT
NLRP3 Inflammasome Inducer - Silicon Dioxid Nanoparticles
SiO2 nanoparticles (Nano-SiO2) are single particles of silica dioxide, an inorganic metal oxide, with a diameter of less than 100 nm.
Several studies have demonstrated that Nano-SiO2 trigger the NLRP3 inflammasome-dependent induction of interleukin-1β (IL-1β) and IL-18 in vitro and in vivo [1,2].
The biological activity of Nano-SiO2 has been validated using InvivoGen's THP-1 Null cells and HEK-Blue™ IL-1β cells.
Key features:
- Potent inducer of the NLRP3 inflammasome
- Nanoparticles with a diameter of <100 nm
- Each lot is functionally tested
Read our review on the NLRP3 inflammasome.
Download our Practical guide on Inflammasomes.
References:
1. Nakayama M. et al., 2018. Macrophage recognition of crystals and nanoparticles. Front Immunol. 9:103.
2. He Y. et al., 2016. NEK7 is an essential mediator of NLRP3 activation downstream of potassium efflux. Nature. 530(7590):354-7.
All products are for research use only, and not for human or veterinary use.
InvivoGen also offers:
SPECIFICATIONS
Specifications
SiO2
10-250 µg/ml
Cellular assays
Biological activity validated using cellular assays, Absence of bacterial contamination (e.g. lipoproteins and endotoxins) confirmed using HEK-Blue™ TLR2 and HEK-Blue™ TLR4 cells.
CONTENTS
Contents
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Product:Nano-SiO2
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Cat code:tlrl-sio-2
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Quantity:20 mg (2 x 10 mg)
Shipping & Storage
- Shipping method: Room temperature
- Room temperature
Storage:
Details
The NLRP3 inflammasome is an intracellular multi-protein complex that plays a central role in innate immunity. It is activated by a two-step process. A first signal (‘priming’) is provided by pathogen-associated molecular patterns (PAMPs) or cytokines. It allows the transcriptional upregulation of key inflammasome actors and the post-translational modification of NLRP3 . The second signal (‘activation’) is provided by a wide array of stimuli including microbial toxins, endogenous molecules or crystalline substances. The current paradigm is that NLRP3 does not bind directly to these molecules. Rather it senses downstream cytosolic stress signals such as K+ efflux. This triggers inflammasome multimerization and pro-caspase-1 maturation. Proximity-induced autolytic activation of caspase-1 leads to the formation of gasdermin D (GSDMD) pores at the cell surface, allowing IL-1β/IL-18 and alarmin secretion, and ultimately, pyroptosis [1,2].
References:
1. Swanson K.V. et al., 2019. The NLRP3 inflammasome: molecular activation and regulation to therapeutics. Nat. Rev. Immunol. 19:477.
2. Groslambert M. & Py B. 2018. Spotlight on the NLRP3 inflammasome pathway. J. Inflamm. Res. 11:359.
DOCUMENTS
Documents
Technical Data Sheet
Safety Data Sheet
Validation Data Sheet
Certificate of analysis
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