a bZIP transcription factor that coordinates proliferation arrest and the differentiation of myeloid progenitors, adipocytes, hepatocytes, and cells of the lung and the placenta.
C/EBP-alpha and -beta play essential and redundant functions during early embryogenesis. Forms homodimers or heterodimers with C/EBP-beta and -gamma. Required for postnatal maintenance of systemic energy homeostasis and lipid storage. Downregulates the expression of genes that maintain cells in an undifferentiated and proliferative state through E2F1 repression, which is critical for its ability to induce adipocyte and granulocyte terminal differentiation. Proliferation arrest also depends on a functional binding to SWI/SNF complex. In liver, regulates gluconeogenesis and lipogenesis through different mechanisms. To regulate gluconeogenesis, functionally cooperates with FOXO1 binding to IRE-controlled promoters and regulating the expression of target genes such as PCK1 or G6PC. To modulate lipogenesis, interacts and transcriptionally synergizes with SREBF1 in promoter activation of specific lipogenic target genes such as ACSS2. In adipose tissue, seems to act as FOXO1 coactivator accessing to adiponectin promoter through FOXO1 binding sites. Mutated in 9% of patients with acute myeloid leukemia (AML). The human protein has four isoforms produced by alternative initiation sites. Isoform 3 (p30) promotes the maintenance of an undifferentiated cellular state. Isoform 4 directly and specifically enhances ribosomal DNA transcription interacting with RNA polymerase I-specific cofactors and inducing histone acetylation. Mutations that favor expression of isoform 3 are the most common type of C/EBPa mutation in AML. Isoform 3 preferentially interacts with Wdr5, inhibiting differentiation and promoting the development of SET/MLL (SET-domain/mixed-lineage leukemia). Note: This description may include information from UniProtKB.