Heike L. Pahl

TL;DR: It is argued that NF-κB functions more generally as a central regulator of stress responses and pairing stress responsiveness and anti-apoptotic pathways through the use of a common transcription factor may result in increased cell survival following stress insults.

TL;DR: The data suggest that such diverse stimuli as OA, TNF and PMA use the same kinase system to phosphorylate and thereby destabilize I kappa B‐alpha, leading to NF‐kappa B activation.

TL;DR: In this article, the authors reported an alternative mechanism of NF-κB activation by using tyrosine-phosphorylation of IκB-α in the presence of pervanadate.

TL;DR: It is shown that internal stress, caused by the accumulation of proteins in the endoplasmic reticulum, also induces NF‐kappa B DNA binding as well as kappa B‐dependent gene expression and participates in a novel ER‐nuclear signal transduction pathway distinct from the unfolded‐protein‐response described previously.

TL;DR: It is reported here that JAK2V617F-associated disease is strongly associated with a specific constitutional Jak2 haplotype, designated 46/1, in all three disease entities compared to healthy controls and provides a model whereby a constitutional genetic factor is associated with an increased risk of acquiring a specific somatic mutation.