Nikoleta Batchvarova

TL;DR: Compared with the wild type, mouse embryonic fibroblasts derived from chop -/- animals exhibited significantly less programmed cell death when challenged with agents that perturb ER function, and the proximal tubule epithelium of chop -/+ animals exhibited fourfold lower levels of TUNEL-positive cells, and significantly less evidence for subsequent regeneration.

TL;DR: Comparing the complement of genes expressed in stressed wild‐type mouse embryonic fibroblasts with those expressed in cells nullizygous for chop reveals the existence of a novel CHOP‐dependent signaling pathway, distinct from the known endoplasmic reticulum unfolded protein response, which may mediate changes in cell phenotype in response to stress.

TL;DR: The data suggest that CHOP functions as an inducible inhibitor of adipocytic differentiation in response to metabolic stress by interfering with the accumulation of adipogenic C/EBP isoforms.

TL;DR: The identification of a positively regulated direct CHOP-C/EBP target gene, that encoding murine carbonic anhydrase VI (CA-VI), is described, which points to a preeminent role for CHOP in CA-VI induction during stress.

TL;DR: Regulation of the k10 gene is examined in keratinocytes in the skin of normal mice and in transgenic mice carrying targeted deletions of c/ebpbeta and ap-2alpha to support a regulatory model in which C/EBPbeta activates and maintains AP-2 expression in basal keratin cells, whereas AP- 2 represses C/EBPalpha in those cells.