The major finding was that IKKβ phosphorylation increased exclusively after resistance exercise.

We provide genetic evidence that Tak1 is essential for Tax-induced IKK activation.

The synthesis and biological activities of these potent IKK inhibitors are described.

Further, pharmacological inhibition of IKKβ also blocked human adipose stem cell differentiation.

Whether IKK also participates in other signaling events is not known.

Here we show that Tax modulates the cellular localization of the IKK complex.

IKKβ has previously been implicated in breast cancer bone metastasis and bone remodelling.

Pretreatment with CM with CLA attenuated the increased IKK activity induced by H. pylori.

Our findings provide insights into IKK activation and how pathogens subvert host-cell signaling pathways.

Nuclear Factor Kappa B levels were increased in BAT, whereas Ikk-γ levels increased in WAT.

The gene codes for a certain kind of a protein, a kinase known as IKK-epsilon.

However, existing IKKβ inhibitors are known to induce paradoxical immune activation, which limits their clinical usefulness.

Further, chronic treatment of mice with a potent IKKβ inhibitor decreased adipogenesis and ameliorated diet-induced obesity.

Our findings provide the first direct link between LRRK2 and the IKKs that mediate many immune responses.

When the scientists prevented laboratory-grown cancer cells from making IKK-epsilon, the cells stopped growing or even died.

We investigated whether mice that express an activated form of IKKβ in the esophageal epithelia develop esophageal disorders.