Cold shock domain factors activate the granulocyte-macrophage colony-stimulating factor promoter in stimulated Jurkat T cells

Cold shock domain (CSD) family members have been shown to play roles in either transcriptional activation or repression of many genes in various cell types. We have previously shown that CSD proteins dbpAv and dbpB (also known as YB-1) act to repress granulocyte-macrophage colony-stimulating factor transcription in human embryonic lung (HEL) fibroblasts via binding to single-stranded DNA regions across the promoter. Here we show that the same CSD factors are involved in granulocyte-macrophage colony-stimulating factor transcriptional activation in Jurkat T cells. Unlike the mechanisms of CSD repression in HEL fibroblasts, CSD-mediated activation in Jurkat T cells is not mediated through DNA binding but presumably through protein-protein interactions via the C terminus of the CSD protein with transcription factors such as RelA/NF-kappaB p65. We demonstrate that Jurkat T cells lack truncated CSD factor subtypes present in HEL fibroblasts, which raises the possibility that the cellular content of CSD proteins may determine their final role as activators or repressors of transcription.