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.
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.
Digital NF-κB signaling achieves orthogonal control over the probability of activation (percentage of activated cells) and dynamic response heterogeneity in the population via the area and shape of the input profile.
TRAF3, a negative regulator of noncanonical NF-κB signaling, maintains epithelial cell quiescence at confluence, and its loss triggers upregulation of immunity genes and prevents entry into G0 at high cell density.
β-Catenin-mediated expansion of nephron progenitors is independent of direct β-catenin/chromatin engagement, while progenitor induction proceeds with a β-catenin-driven switch of repressive TCFL1/TCFL2 to activating TCF7/LEF1 factors on transcriptionally poised enhancers.
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.
Sustained TNF-α induction consolidates transcriptional memory for faster, stronger, and more sensitive subsequent induction in an active DNA demethylation-dependent manner for memory genes including CALCB, a therapeutic target for migraine.