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NOD1 Agonist - D-gamma-Glu-mDAP
γ-D-Glu-mDAP (iE-DAP) is a dipeptide present in the peptidoglycan (PGN) of all Gram-negative and certain Gram-positive bacteria. iE-DAP is the minimal motif recognized by the intracellular receptor NOD1.
Recognition of iE-DAP by NOD1 induces NF-κB activation and the production of inflammatory cytokines. iE-DAP provided by InvivoGen is chemically synthesized and tested using HEK-Blue™ NOD1.
Note: iE-DAP is a mixture of γ-D-Glu-D-mDAP and γ-D-Glu-L-mDAP.
Specificity: NOD1 agonist
Working Concentration: 1 - 100 µg/ml
Endotoxin level: <0.125 EU/ml
Solubility: 10 mg/ml in water
Molecular weight: 319.31
Synonym: γ-D-glutamyl-meso-diaminopimelic acidBack to the top
iE-DAP is provided as a sterile white lyophilized powder.
- 5 mg γ-D-Glu-mDAP (iE-DAP)
- 2 ml sterile endotoxin-free water
iE-DAP is shipped at room temperature.
Store at -20°C. Upon resuspension, aliquote iE-DAP and store at -20°C.
Product is stable 1 year at -20°C when properly stored.
Avoid repeated freeze-thaw cycles.Back to the top
γ-D-Glu-mDAP (iE-DAP) is a dipeptide present in the peptidoglycan (PGN) of a subset of bacteria that include Gram-negative bacilli and particular Gram-positive bacteria such as Bacillus subtilis and Listeria monocytogenes .
iE-DAP is the minimal motif recognized by NOD1 (CARD4), an intracellular sensor expressed in multiple tissues including intestinal epithelia cells. Recognition of iE-DAP by NOD1 induces a signaling cascade involving the serine/threonine RIP2 (RICK, CARDIAK) kinase which interacts with IKK leading to the activation of NF-κB and the production of inflammatory cytokines such as TNF-α and IL-6 .
iE-DAP provided by InvivoGen is chemically synthesized and tested using HEK-Blue™ NOD1.
Note: iE-DAP is a mixture of γ-D-Glu-D-mDAP and γ-D-Glu- L-mDAP.
1. Chamaillard M. et al., 2003. An essential role for NOD1 in host recognition of bacterial peptidoglycan containing diaminopimelic acid. Nat. Immunol.4(7):702-7
2. Park JH. et al., 2007. RICK/RIP2 mediates innate immune responses induced through Nod1 and Nod2 but not TLRs. J Immunol. 178(4):2380-6.