In the context of gene regulation: transactivation is the increased rate of gene expression triggered either by biological processes or by artificial means, through the expression of an intermediate transactivator protein.
Transactivation can be triggered either by endogenous cellular or viral proteins, also called transactivators. These protein factors act in trans (i.e., intermolecularly). HIV and HTLV are just two of the many viruses that encode transactivators to enhance viral gene expression. These transactivators can also be linked to cancer if they start interacting with, and increasing expression of, a cellular proto-oncogene. HTLV, for instance, has been associated with causing leukemia primarily through this process. Its transactivator, Tax, can interact with p40, inducing overexpression of interleukin 2, interleukin receptors, GM-CSF and the transcription factor c-Fos. HTLV infects T-cells and via the increased expression of these stimulatory cytokines and transcription factors, leads to uncontrolled proliferation of T-cells and hence lymphoma.
Artificial transactivation of a gene is achieved by inserting it into the genome at the appropriate area as transactivator gene adjoined to special promoter regions of DNA. The transactivator gene expresses a transcription factor that binds to specific promoter region of DNA. By binding to the promoter region of a gene, the transcription factor causes that gene to be expressed. The expression of one transactivator gene can activate multiple genes, as long as they have the same, specific promoter region attached. Because the expression of the transactivator gene can be controlled, transactivation can be used to turn genes on and off. If this specific promoter region is also attached to a reporter gene, we can measure when the transactivator is being expressed.
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For instance,there are indications that both D1 and D2 receptors can trans-activate the brain-derived neurotrophic factor (BDNF) receptor in neurons (Swift et al., 2011). These two dopamine receptors can also regulate calcium channels through a direct protein–protein interaction in vivo (Kisilevsky and Zamponi, 2008; Kisilevsky et al., 2008). Direct interaction of D1 and D2 receptors and Na+-K+-ATPase has also been demonstrated (Hazelwood et al., 2008; Blom et al., 2012).