TRAM is a regulator of myddosome assembly through dissociating MyD88 from the TLR–TIRAP complex to enable myddosome maturation and durable downstream signal transduction.

Wang et al. report that the cell cycle regulators CDK4/6 also regulate the inflammatory phenotype of senescent cells, via modulation of retinoic acid signaling and NF-κB. Pharmacologically targeting t...

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Shiya Lin — the URECA researcher of the month for June — is a double major in biology and psychology who has been working in the Mallipattu Lab in the Department of Medicine, Division of Nephrology an...

Read the full paper: Reduced SH3RF3 May Protect Against Alzheimer's Disease by Lowering Microglial Pro-Inflammatory Responses via Modulation of JNK and NFkB Signaling

Influenza A virus (IAV) is an important zoonotic pathogen responsible for substantial respiratory morbidity and mortality. Elucidating the mechanisms by which IAV evades host innate immunity is cri...

The nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) family regulates fundamental processes in both innate and adaptive immunity. Aberrant NF-κB activation, whether through canonical or non-canonical signaling pathways, contributes to chronic inflammation, autoimmunity, allergy, and primary immunodeficiency/autoinflammatory syndromes, while also influencing host defense and tissue repair mechanisms. The present review aims to synthesize molecular architecture, upstream triggers, ubiquitin-centered relay systems, and the dynamic regulation of NF-κB activity. The major findings on the NF-κB signaling pathway encompass its dual molecular mechanisms (canonical and non-canonical), its central roles in immune and inflammatory responses, cell survival, and development, as well as its complex regulatory networks. We interpret NF-κB as a master integrator of diverse signals, essential for both acute and long-term physiological processes. Dysregulation of NF-κB underlies many diseases, and while it is a promising therapeutic target, its ubiquitous functions demand precise modulation to avoid adverse effects. In conclusion, the proper function of the NF-κB signaling pathway is essential for maintaining cellular homeostasis and immune defense; its dysregulation is linked to chronic inflammatory diseases, autoimmune disorders, and cancer, which underscores the pathway’s significance as a therapeutic target. Although it elucidates molecular processes and treatment options, experimental validation of emerging therapeutic concepts such as ubiquitin code editing and spatial immunology remains limited.