MSU Crystals - NLRP3 Inflammasome Inducer

Monosodium Urate Crystals

ABOUT

NLRP3 inflammasome Inducer - Monosodium Urate Crystals

Monosodium urate (MSU) crystals are the aetiological agent of the acute inflammatory condition gout. They act as a key danger-associated molecular patterns (DAMPs) able to stimulate the NLRP3 inflammasome-dependent induction of interleukin-1β (IL-1β) and IL-18 [1].

More details

 

The biological activity of MSU crystals has been validated using InvivoGen's THP1-HMGB1-Lucia™ cells and HEK-Blue™ IL-1β cells.

Key features:

  • Potent inducer of the NLRP3 inflammasome
  • Each lot is functionally tested

 

Read our review on the NLRP3 inflammasome.

Download our Practical guide on Inflammasomes.

 

Reference:

1. Martinon F. et al., 2006. Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature. 440(7081):237-41.

All products are for research use only, and not for human or veterinary use.

SPECIFICATIONS

Specifications

CAS number
1198-77-2
Chemical formula

C5H3N4NaO3

Molecular weight
190.1 g/mol
Working concentration

100 - 200 µg/ml

Solubility

Not soluble

Quality control

Each lot is functionally tested

CONTENTS

Contents

  • Product: 
    MSU Crystals
  • Cat code: 
    tlrl-msu
  • Quantity: 
    5 mg
Includes:

tlrl-msu: 5 mg

Shipping & Storage

  • Shipping method:  Room temperature
  • Storage:

    • 4°C or -20°C

    Caution:

    • Avoid repeated freeze-thaw cycles

Details

MSU crystals act as endogenous danger signals that stimulate the innate immune system to produce inflammatory cytokines such as IL-1β. Engagement of the NRLP3 inflammasome is supported by the finding that macrophages from mice deficient in various components of the inflammasome did not respond to injection of MSU crystals [1].

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 [2,3].

 

References:

1. Martinon F. et al., 2006. Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature. 440(7081):237-41.
2. Swanson K.V. et al., 2019. The NLRP3 inflammasome: molecular activation and regulation to therapeutics. Nat. Rev. Immunol. 19:477.
3. Groslambert M. & Py B. 2018. Spotlight on the NLRP3 inflammasome pathway. J. Inflamm. Res. 11:359.

Chemical structure of MSU Crystals:

Chemical structure of MSU Crystals

DOCUMENTS

Documents

MSU Crystals

Technical Data Sheet

Safety Data Sheet

Validation Data Sheet

Certificate of analysis

Need a CoA ?

CUSTOMER SERVICE & TECHNICAL SUPPORT

Question about this product ?