Figure 7. Model for regulation of Alk transcription by estrogen and LMO4. A, Estrogen (through ERα) and LMO4 have opposing effects on Alk levels in Acb and behavioral responses to cocaine. B, Model illustrating the regulation of Alk transcription by LMO4 and ERα. Under conditions of low estrogen or high LMO4, a repressive complex occupies the Alk promoter, resulting in low levels of Alk expression. Conversely, in the presence of estrogen, or if LMO4 levels decrease, repression of the Alk promoter is relieved by recruitment of a coactivator complex to the Alk promoter and Alk levels increase. We hypothesize that LMO4 recruits a histone deacetylase to the complex, since LMO4 is known to interact with HDAC2 in complex with ERα in breast cancer cells, and that ERα interacts with another DNA binding partner, such as SP1, CREB, or the AP1 complex among others (white oval).