Fig. 8: Proposed model of the interplay between CEBPA isoforms, AP-1 factors and external stimuli.
From: Mutant CEBPA promotes tolerance to inflammatory stress through deficient AP-1 activation
p30 is unable to promote normal expression of the FOS gene, leading to deregulation of FOS target genes, including many inflammatory genes. As a consequence, p30-expressing cells have reduced cytokine secretion and cell death compared to p42-expressing cells upon persistent inflammatory stress. We also observe that only the p42 isoform can dimerize with the AP-1 factor ATF4, crucial in the regulation of the ER stress response. Consequently, there is an altered transcriptional activation of ATF4-target genes in p30-expressing cells, making them more sensitive to acute ER stress, and conferring a new potential vulnerability to preferentially eliminate p30-expressing cells.
