Cell imaging and mathematical modelling show reciprocal cross-regulation between inflammatory signalling and cell cycle timing, which is mediated through functional interactions between NF-B and E2F proteins.
By inhibiting the activation of NF-κB, HIV-1 Vpu exerts much broader immunosuppressive effects than previously anticipated and may be an important determinant of chronic inflammation in HIV-1 infected individuals.
By controlling the SUMOylation of the protein CAR-1, the aging-regulating pathways downstream of the Insulin/IGF signaling cascade and of the germ cells of the nematode Caenorhabditis elegans are integrated.
SMAD1/5 signaling is essential for the full transforming growth factor β (TGF-β)-induced transcriptional program and physiological responses and is induced via a novel receptor activation mechanism, involving two distinct type I receptors.
The structure of the Nef:AP-2 complex has been determined and used as the basis of a model that explains how HIV-1 Nef downregulates the CD4 receptor from the surface of the infected cells.
Ligand binding to the ectodomain of the insulin-like growth factor receptor destabilises an autoinhibitory inter-subunit interaction, which allows the transmembrane domains to associate and the intracellular regions to autophosphorylate.
The nuclear protein Sam68 plays a role in the genotoxic stress-initiated "nuclear to cytoplasmic" activation of NF-κB and is involved in the development and survival of colon cancer.
The appearance of NG2+ glial cells in the dorsal telencephalon of the embryo coincides with the establishment of the brain blood vessel network in mice.
