IRAK1 Duplication in MECP2 Duplication Syndrome Does Not Increase Canonical NF-κB-Induced Inflammation.
Ilona GottschalkUwe KölschDimitrios L WagnerJonas KathStefania MartiniRenate KrügerAnne PuelJean-Laurent CasanovaAleksandra Jezela-StanekRainer RossiSalima El ChehadehHilde Van EschHorst Von BernuthPublished in: Journal of clinical immunology (2022)
Patients with MECP2/IRAK1 duplication syndrome do not show increased canonical NF-κB signaling in immortalized fibroblasts, PBMCs, and whole blood. Therefore, we assume that these patients do not benefit from a therapeutic suppression of this pathway.
Keyphrases
- oxidative stress
- end stage renal disease
- signaling pathway
- lps induced
- ejection fraction
- newly diagnosed
- chronic kidney disease
- pi k akt
- case report
- diabetic rats
- prognostic factors
- peritoneal dialysis
- nuclear factor
- high glucose
- inflammatory response
- endothelial cells
- toll like receptor
- cell proliferation
- drug induced
- immune response
- patient reported outcomes