Synergism molecular basis

Does a molecular basis exist for synergism of cisplatin with other drugs ... 

Study of the molecular basis of synergism, i.e. studying the simultaneous effect upon DNA binding (and distortion) of cisplatin in combination with other drugs. 

IL-2 often synergizes with other cytokines (notably IL-12) to induce IFNy production by NK cells and to increase cytotoxicity by NK and LAK cells. The expression of the receptor for this cytokine on NK cells is, however, continuous in character, but only a very small percentage of these cells have receptors of great affinity. The study of differential use of Janus kinase-signal transducer activator of transcription signaling pathways in the stimulation of human NK cells by IL-2, IL-12, and IFNa has demonstrated a differential phosphorylation and consequent differential activation of both separate and overlapping STAT proteins by IL-2, IL-12, and IFNa. This may provide a molecular basis for the similarities and differences in the actions of these cytokines on NK cells. ... 

In vitro observations have demonstrated a marked synergism between PKC and Rho or Arf in the activation of PLDl [11, 56]. The molecular basis of this synergism is unknown, but binding of these regulators to the phospholipase must induce conformational changes that interact to produce enhanced activation. As indicated elsewhere in this chapter, PKC interacts with the N-terminal region of PLDl, but probably has an additional site(s). Rho binds to a sequence in the C-ter-minus, but the site of interaction of Arf is unknown. 

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