The NF-B family mediates immune and inflammatory responses. In many cancers, NF-B is constitutively activated and induces the expression of genes that facilitate tumorigenesis. ING4 is a tumor suppressor that is absent or mutated in several cancers. Herein, we demonstrate that in human gliomas, NF-B is constitutively activated, ING4 expression is negligible, and NF-B-regulated gene expression is elevated. We demonstrate that an ING4 and NF-B interaction exists but does not prevent NF-B activation, nuclear translocation, or DNA binding. Instead, ING4 and NF-B bind simultaneously at NF-B-regulated promoters, and this binding correlates with reductions in p65 phosphorylation, p300, and the levels of acetylated histones and H3-Me3K4, while enhancing the levels of HDAC-1 at these promoters. Using a knockdown approach, we correlate reductions in ING4 protein levels with increased basal and inducible NF-B target gene expression. Collectively, these data suggest that ING4 may specifically regulate the activity of NF-B molecules that are bound to target gene promoters.

The present study set out to repeat and perhaps to verify two very important investigations of the pecking response in chicks. Breed (2), in 1911, studied the accuracy of this response and plotted a development curve from the data of twenty-one chicks over a period of twenty-five days. In 1913, Shepard and Breed (4) compared with the normal development curve as obtained by Breed the development curves obtained from chicks in which the appearance of the pecking response had been artificially delayed for three, four, or five days. Since the findings of these workers, as well as their interpretations, have been extensively accepted and quoted, a repetition of the work under as nearly as possible the same conditions is much to be desired. This is the task which I have undertaken.In repeating these studies the essential problems of fact are as follows: