Mouse TLR7 Reporter HEK 293 Cells

NF-κB-SEAP reporter cells

SPECIFICATIONS

Specifications

Target

TLR7

Target species

Mouse

Tested applications

Detection and quantification of mouse TLR7 activity

Species
Mouse
Cell type
Epithelial
Growth properties
Adherent
Tissue origin
Human embryonic kidney cells
Reporter gene
SEAP
Detection method
Colorimetric
Growth medium

Complete DMEM (see TDS)

Antibiotic resistance
Blasticidin
Zeocin®
Mycoplasma-free

Verified using PlasmotestTM

Quality control

Each lot is functionally tested and validated.

CONTENTS

Contents

  • Product: 
    HEK-Blue™ mTLR7 Cells
  • Cat code: 
    hkb-mtlr7
  • Quantity: 
    3-7 x 10^6 cells
Includes:
  • 1 ml Blasticidin (10 mg/ml)
  • 1 ml Zeocin® (100 mg/ml)
  • 1 ml Normocin™ (50 mg/ml)
  • 1 pouch of HEK-Blue™ Detection (cell culture medium for real-time detection of SEAP)

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

Toll-Like Receptor 7

In humans, four Toll-Like Receptor (TLR) family members TLR3, TLR7, TLR8, and TLR9, mainly found in the endosome, are specialized in sensing viral-derived components. TLR7 and TLR8 recognize single-stranded (ss)RNA structures, such as viral ssRNA, miRNA, and various synthetic agonists [1]. Despite their similarities in PAMP (pathogen-associated molecular pattern) recognition, structure, and signaling partners, they highly differ in expression profiles and signaling responses, with TLR7 being more involved in the antiviral immune response and TLR8 mastering the production of proinflammatory cytokines [2]. TLR7 is mainly found in plasmacytoid dendritic cells (pDCs) and B cells, whereas TLR8 is highly expressed in monocytes, monocyte-derived DCs (mDCs), and macrophages [3].

TLR7 signaling

Upon viral infection, TLR7 translocates from the endoplasmic reticulum via the Golgi into the endosomes. Subsequently, it undergoes proteolytic cleavage and dimerization [1,3]. Once activated, it recruits the adaptor protein MyD88 to trigger IRF, AP-1, and NF-kB responses via TRAF6 (TNF receptor-associated factor 6) [1,3]. Depending on the stimulus and cell type, TLR7-mediated signaling induces IFN-α and IFN-regulated cytokines or T helper 17 (Th17) polarizing cytokines, such as interleukin (IL)-1β and IL-23 [4].

TLR7 therapeutic targeting

The involvement of nucleic acid-sensing mechanisms in the immune response against infections and other diseases makes them interesting targets for drug design [4]. TLR7 agonists are currently been tested as vaccine adjuvants and immunomodulatory therapeutics. They are extensively studied in the context of viral infection (e.g. SARS-CoV-2, Influenza, HIV), autoimmune (e.g. asthma, Lupus), and autoinflammatory diseases (e.g. cancer) [1-4]. Understanding the fundamental differences between these two related receptors could potentially be harnessed to discover novel drugs and improve vaccine efficacy/safety [4].

 

​References:

1. Martínez-Espinoza I & Guerrero-Plata A. 2022. The Relevance of TLR8 in Viral Infections. Pathogens. 11(2):134.
2. Salvi V, et al., 2021. SARS-CoV-2-associated ssRNAs activate inflammation and immunity via TLR7/8. JCI Insight.;6(18):e150542.
3. Georg P. & Sander L.E., 2019. Innate sensors that regulate vaccine responses. Curr. Op. Immunol. 59:31.
4. de Marcken M, et al., 2019. TLR7 and TLR8 activate distinct pathways in monocytes during RNA virus infection. Sci Signal.;12(605):eaaw1347.  

DOCUMENTS

Documents

HEK-Blue™ mTLR7 Cells

Technical Data Sheet

Validation Data Sheet

Safety Data Sheet

Certificate of analysis

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