Notification: Reference #hkb-hnod2v2-av can only be ordered together with reference #hkb-hnod2v2.

Human NOD2 expressing HEK293 reporter cells

Signaling pathways in HEK-Blue™ hNOD2 cells

HEK-Blue™ hNOD2 cells were engineered from the human embryonic kidney HEK 293 cell line to assess the role of the Nucleotide-binding Oligomerization Domain-containing protein 2 (NOD2).

These cells stably express the human NOD2 gene and an NF-κB-inducible SEAP reporter gene. SEAP (secreted embryonic alkaline phosphatase) activity upon NOD2 stimulation can be readily determined by performing the assay in HEK-Blue™ Detection. This cell culture medium allows for real-time detection of SEAP. Alternatively, SEAP activity may be monitored using QUANTI-Blue™, a SEAP detection reagent.

The overexpression of hNOD2 renders HEK-Blue™ hNOD2 cells to strongly respond to NOD2-specific ligands. As HEK293 cells express endogenous levels of TLR3 and TLR5, these cells will respond to their cognate ligands such as Poly(I:C) and flagellin. However, these cells are unresponsive to NOD1-specific ligands, such as Tri-DAP (see figures).

NOD1 and NOD2 are cytosolic pattern recognition receptors (PRRs), specialized to sense distinct motifs of peptidoglycan, an essential constituent of the bacterial cell wall. NOD2 recognizes the muramyl dipeptide (MDP) structure found in almost all bacteria, acting as a general sensor of bacterial invasion [1].

More details

Key Features:

Stable expression of human NOD2
Unresponsive to NOD1-ligands
Strong and stable response to NOD2-specific ligands
Distinct monitoring of NF-κB by assessing the SEAP activities

Applications:

Defining the distinct role of NOD2 in the NF-κB-dependent pathway
Screening for NOD2-specific agonists or inhibitors in comparison with their parental cell line HEK-Blue™ Null2

Note: A new clone is provided with an improved hNOD2 response. The cat code has been changed accordingly (hkb-hnod2v2).

References:

1. Correa RG, Milutinovic S, Reed JC,. 2012. Roles of NOD1 (NLRC1) and NOD2 (NLRC2) in innate immunity and inflammatory diseases. Biosci Rep. 32(6):597-608.

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