An international collaboration between the Institute of Biomedical Research of Barcelona Science Park, the Biomedical Research Institute Alberto Sols CSIC and the Institute of Molecular Cardiology Research in Boston, have observed that inhibition of the route of the N-terminal kinase factor c-Jun, implicated in cell proliferation. The inhibitory action of glucocorticoids on the route of this kinase (JNK) represses the transcription factor AP-1, which is part of c-Jun. The term AP-1 (activator protein 1) refers to dimeric transcription factors composed of subunits Jun, Fos or ATF (activating transcription factor) that bind to a common DNA binding, the binding site AP-1 .

The antagonism between glucocorticoids and AP-1 factor is based primarily on the role of repression of the glucocorticoid receptor (GR), mediate essential physiological and pharmacological functions. The authors show that glucocorticoids induce the dissociation of JNK kinase 7 of the mitogen-activated protein kinase (MKK7) by promoting its association with the GR receptor and have characterized structurally GR-JNK interaction, a union which is required for inactivation JNK nuclear transfer of this kinase in an inactive form. The nuclear accumulation of inactive JNK may be relevant to enhance the repression of AP-1 activities by glucocorticoids.