Maeran Uhm

TL;DR: The authors showed that amlexanox, currently used to treat asthma and canker sores, is a relatively specific inhibitor of the noncanonical IκB kinases IKK-α and TANK-binding kinase 1 (TBK1) and that it improves metabolic disease in mouse genetic and dietary models of obesity.

TL;DR: It is reported that the kinase uniquely controls energy metabolism, and a unique role for TBK1 in mediating bidirectional crosstalk between energy sensing and inflammatory signaling pathways in both over- and undernutrition.

TL;DR: It is suggested that by reducing production of cAMP in adipocytes, IKKε and TBK1 may contribute to the repression of energy expenditure during obesity.

TL;DR: It is shown that acute inhibition of IKK-ε and TBK1 with amlexanox treatment increases cAMP levels in subcutaneous adipose depots of obese mice, promoting the synthesis and secretion of the cytokine IL-6 from adipocytes and preadipocytes, but not from macrophages.

TL;DR: Data indicate that TBK1 controls GLUT4 vesicle engagement and disengagement from the exocyst, suggesting that exocySt components not only constitute a tethering complex for the GLUT 4 vesicles but also act as “gatekeepers” controlling vesicular fusion at the plasma membrane.