Mouse ASC-expressing RAW 264.7 Cells

ASC-OE mouse macrophages

SPECIFICATIONS

Specifications

Tested applications

Inflammasome cellular assays

Species
Mouse
Cell type
Monocytic
Growth properties
Adherent
Tissue origin
Mouse macrophages
Growth medium

Complete DMEM (see TDS)

Antibiotic resistance
Blasticidin
Mycoplasma-free

Verified using Plasmotest™

Quality control

Each lot is functionally tested and validated.

CONTENTS

Contents

  • Product: 
    RAW-ASC Cells
  • Cat code: 
    raw-asc
  • Quantity: 
    3-7 x 10^6 cells
Includes:
  • 1 ml of Normocin™ (50 mg/ml)
  • 1 ml of Blasticidin (10 mg/ml)

Shipping & Storage

  • Shipping method:  Dry ice
  • Storage:

    • Liquid nitrogen vapor
    Stability: 20 passages

    Caution:

    • Upon receipt, store immediately in liquid nitrogen vapor. Do not store cell vials at -80°C.

Details

Inflammasomes are multimeric protein complexes that are crucial for host defense against infection and response to endogenous danger signals. The canonical inflammasome response is driven by aggregation of a sensor (i.e. NLRP3) with the ASC adaptor and pro-caspase-1. Activation of caspase-1 (CASP1) induces the maturation of pro-IL-1β/pro-IL-18 and cleavage of the pore-forming protein gasdermin D (GSDMD), leading to secretion of IL-1β/ 18 and pyroptosis. 

ASC is essential to inflammasome sensors that do not contain a CARD domain, such as NLRP3, AIM2, and Pyrin [1]. This is due to the bipartite composition of ASC, consisting of one PYD and one CARD domain, allowing the recruitment of the CARD-containing pro-caspase-1 to these sensors. Whereas, the NLRP1 and NLRC4 inflammasome sensors have a CARD domain, and can recruit pro caspase-1 either directly or through ASC. However, it has been shown that upon activation of these sensors, in the absence of ASC, the secretion of mature IL-1β and IL-18 is reduced [1]. As the non-canonical inflammasome (i.e. CASP4/5/11) can not directly activate CASP1, they trigger GSDMD-driven release of alarmins and K+ efflux to induce the activation of NLRP3 and CASP1-mediated IL-1β/-18 maturation and secretion. Therefore, the absence of ASC affects the downstream inflammatory signaling from the non-canonical inflammasome also. 

 

1. Mathur A. et al., 2017. Molecular mechanisms of inflammasome signaling. J. Leuk. Biol. 103:233.

DOCUMENTS

Documents

RAW-ASC Cells

Technical Data Sheet

Validation Data Sheet

Safety Data Sheet

Certificate of analysis

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