The primary cilium influences interleukin-1 beta-induced NF kappa B signalling by regulating IKK activity

AbstractThe primary cilium is an organelle acting as a master regulator of cellular signalling. We have previously shown that disruption of primary cilia assembly, through targeting intraflagellar transport, is associated with muted nitric oxide and prostaglandin responses to the inflammatory cytokine interleukin-1β (IL-1β). Here, we show that loss of the primary cilium disrupts specific molecular signalling events in cytosolic NFκB signalling. The induction of cyclooxygenase 2 (COX2) and inducible nitrous oxide synthase (iNOS) protein is abolished. Cells unable to assemble cilia exhibit unaffected activation of IκB kinase (IKK), but delayed and reduced degradation of IκB, due to diminished phosphorylation of inhibitor of kappa B (IκB) by IKK. This results in both delayed and reduced NFκB p65 nuclear translocation and nuclear transcript binding. We also demonstrate that heat shock protein 27 (hsp27), an established regulator of IKK, is localized to the ciliary axoneme and cellular levels are dramatically disrupted with loss of the primary cilium. These results suggest that the primary cilia compartment exerts influence over NFκB signalling. We propose that the cilium is a locality for regulation of the molecular events defining NFκB signalling events, tuning signalling as appropriate

Scattering of halo nuclei on heavy targets at energies around the Coulomb barrier : The case of 11Be on 197Au

This work reports on the scattering of 11Be on 197Au at energies around and below the Coulomb barrier. By experimentally identifying the elastic scattering, inelastic scattering and breakup channels, and comparing them with different calculations, valuable information on the 11Be structure and its B(E1) distribution to the continuum are obtained. On top of that, a deeper understanding of the scattering process at low energies is achieved for reactions of this kind, making these studies extendable to other loosely-bound systems like 17,19

Lack of tumor-promoting effects of flavonoids: Studies on rat liver preneoplastic foci and on in vivo and in vitro gap junctional intercellular communication

54 ref.International audienc