In the case of Csrp1, expression analyses and DNA-binding studies indicate that MTF-1 is required for cadmium induction by binding to an MRE upstream of the transcription start. Studies with human, avian and chicken CSRP1 have shown that this protein is localized at adhesion plaques and in association with filamentous actin, and interacts with the adhesion plaque protein zyxin, as well as the actin-cross-linking protein alpha-actinin (54–57). The ability to bind these partners suggests a role in cytoskeletal organization (58). Exposure of cultured cells to cadmium causes a decrease in, and destruction of, cellular contact proteins and the actin cytoskeleton (59). In the proximal tubule cells of the rat kidney, a partial loss of actin and the actin-bundling protein villin is observed upon cadmium treatment, as well as the derangement and depolymerization of microtubules (60). Assuming that CSRP1 is important for the organization of cytoskeletal elements in the mouse, its upregulation by cadmium might protect the organism from damage of the cytoskeleton. Such a mechanism would expand the role of MTF-1 in stress response.