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.
Secretion of the inflammatory cytokine TNF requires a protein called iTAP/FrmD8, which controls the cell surface stability of the TNF shedding machinery, iRhom2 and TACE/ADAM17.
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.
The universal bacteria cell wall component peptidoglycan impacts the egg-laying behavior of infected Drosophila females by directly modulating the activity of few brain octopaminergic neurons.
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.
