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1 The major finding was that IKK β phosphorylation increased exclusively after resistance exercise.
2 We provide genetic evidence that Tak1 is essential for Tax-induced IKK activation.
3 The synthesis and biological activities of these potent IKK inhibitors are described.
4 Further, pharmacological inhibition of IKK β also blocked human adipose stem cell differentiation.
5 Whether IKK also participates in other signaling events is not known.
6 Here we show that Tax modulates the cellular localization of the IKK complex.
7 IKK β has previously been implicated in breast cancer bone metastasis and bone remodelling.
8 Pretreatment with CM with CLA attenuated the increased IKK activity induced by H. pylori.
9 Our findings provide insights into IKK activation and how pathogens subvert host-cell signaling pathways.
10 Nuclear Factor Kappa B levels were increased in BAT, whereas Ikk -γ levels increased in WAT.
11 The gene codes for a certain kind of a protein, a kinase known as IKK - epsilon .
12 However, existing IKK β inhibitors are known to induce paradoxical immune activation, which limits their clinical usefulness.
13 Further, chronic treatment of mice with a potent IKK β inhibitor decreased adipogenesis and ameliorated diet-induced obesity.
14 Our findings provide the first direct link between LRRK2 and the IKKs that mediate many immune responses.
15 When the scientists prevented laboratory-grown cancer cells from making IKK - epsilon , the cells stopped growing or even died.
16 We investigated whether mice that express an activated form of IKK β in the esophageal epithelia develop esophageal disorders.
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