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Inhibitor of nuclear factor kappa-B kinase subunit beta (IKK β) is one of important kinases in inflammation to phosphorylate inhibitor of nuclear factor kappa-B (I κ B α) and then activate nuclear factor kappa-B (NF- κ B). Inhibition of IKK β has been a therapeutic strategy for inflammatory and autoimmune diseases. Here we report that IKK β is constitutively activated in healthy donors and healthy Ikkβ C46A (cysteine 46 mutated to alanine) knock-in mice although they possess intensive IKK β –I κ B α –NF- κ B signaling activation. These indicate that IKK β activation probably plays homeostatic role instead of causing inflammation. Compared to Ikkβ WT littermates, lipopolysaccharides (LPS) could induce high mortality rate in Ikkβ C46A mice which is correlated to breaking the homeostasis by intensively activating p-I κ B α –NF- κ B signaling and inhibiting phosphorylation of 5ʹ adenosine monophosphate-activated protein kinase (p-AMPK) expression. We then demonstrated that IKK β kinase domain (KD) phosphorylates AMPK α 1 via interacting with residues Thr183, Ser184, and Thr388, while IKK β helix–loop–helix motifs is essential to phosphorylate I κ B α according to the previous reports. Kinase assay further demonstrated that IKK β simultaneously catalyzes phosphorylation of AMPK and I κ B α to mediate homeostasis. Accordingly, activation of AMPK rather than inhibition of IKK β could substantially rescue LPS-induced mortality in Ikkβ C46A mice by rebuilding the homeostasis. We conclude that IKK β activates AMPK to restrict inflammation and IKK β mediates homeostatic function in inflammation via competitively phosphorylating AMPK and I κ B α. The dual and opposite role of inhibitor of nuclear factor kappa-B kinase subunit beta (IKK β) restricts and induces inflammation by phosphorylating 5ʹ adenosine monophosphate-activated protein kinase (AMPK) and inhibitor of nuclear factor kappa-B (I κ B α). [Display omitted] [ABSTRACT FROM AUTHOR]

Carbon and water cycles in forest ecosystems are tightly coupled, but global warming-induced soil and atmospheric droughts alter the coupling, thereby greatly increasing uncertainty in predicting carbon and water cycles. Therefore, a carbon–water coupled model (TRIPLEX-CW-Flux) was developed, and an R package (rTRIPLEXCWFlux) was created to facilitate model application. TRIPLEX-CW-Flux integrates vapor pressure deficit and soil moisture into a stomatal conductance submodule to estimate forest carbon and water fluxes. Prediction accuracy of TRIPLEX-CW-Flux and rTRIPLEXCWFlux application were evaluated in a Chinese fir (Cunninghamia lanceolata) plantation. Simulated net ecosystem production (NEP) and evapotranspiration (ET) were in good agreement with flux observations (R 2 : 0.76 for NEP ; 0.71 for ET). Thus, the TRIPLEX-CW-Flux model can be used to predict and quantify effects of global warming-induced droughts on forest carbon and water cycles. The open-access rTRIPLEXCWFlux package facilitates estimations of carbon sequestration and water consumption in forest ecosystems using the observed flux data. • A physiological process model that couples carbon and water flux was developed. • Both atmospheric and soil drought stress were also integrated into the model. • An R package was encoded for the model to predict forest carbon and water flux. • The simulated values were comparable to the flux data observed in the forest. • This R package can be used to evaluate forest functions under climate change. [ABSTRACT FROM AUTHOR]