Glucocorticoids may regulate gene expression in several ways. Glucocorticoids enter the cell to bind to glucocorticoid receptors in the cytoplasm. The resultant GR homodimers translocate to the nucleus. GR homodimers then bind to glucocorticoid-response elements (GRE) in the promoter region of steroid-sensitive genes, which may encode anti-inflammatory proteins. Less commonly, GR homodimers interact with negative GREs to suppress genes, particularly those linked to side effects of glucocorticoids. Nuclear GR also interact with coactivator molecules, such as CREB-binding protein (CBP), which is activated by proinflammatory transcription factors, such as nuclear factor-kB (NF-kB), thus switching off the inflammatory genes that are activated by these transcription factors.