AP-1 family transcription factor that controls the differentiation of lineage-specific cells in the immune system. Selectively suppresses CCN1 transcription and hence blocks the downstream cell proliferation signals produced by CCN1 and inhibits CCN1-induced anchorage-independent growth and invasion in several cancer types. Possibly acts by interfering with AP-1 binding to CCN1 promoter (By similarity). Following infection, participates in the differentiation of CD8(+) thymic conventional dendritic cells in the immune system. Acts via the formation of a heterodimer with JUN family proteins that recognizes and binds DNA sequence 5'-TGA[CG]TCA-3' and regulates expression of target genes. Heterodimer; heterodimerizes with JUN family proteins. By cytokines in response to infection. By IFN-gamma. Mice display normal development of natural killer (NK), T- and B-cells, plasmacytoid dendritic cells (pDCs), neutrophils, resting CD8-alpha(+) classical dendritic cells (cDCs), and peritoneal, liver and lung macrophages. However, they show significantly decreased survival after infection by T.gondii. Notably, mice show significantly decreased numbers of lung-resident CD103(+)CD11b(-) dendritic cells and CD103(+)CD11b(-) macrophages after infection. Belongs to the bZIP family.