The C-terminal peptide of p90rsk can disrupt the interaction of p42/p44 MAPKs with their nuclear phosphatases, thus preventing nuclear p42/p44 MAPKs inactivation. The C-terminal peptide of p90rsk can disrupt the interaction of p42/p44 MAPKs with their nuclear phosphatases, thus preventing nuclear p42/p44 MAPKs inactivation. (A) Alignment of the amino acid sequences of the peptide corresponding to the docking site for p42/p44 MAPKs on p90rsk used in microinjection, the control peptide with the mutated residues shown in green and the docking sites on MKP1, MKP2 and MKP3 with the critical positively charged residues shown in red. (B) In vitro test of the inhibition of the MKP3 activity by the BSA-coupled peptides, the free peptides or BSA alone. (C) Nuclear microinjection of BSA-p90rskwt peptide (a,b,c,d) or BSA-p90rskmut peptide (e,f). Indirect immunofluorescence detection was performed either with the polyclonal antibody anti-BSA (green; a,b,e) or with the monoclonal antibody anti-activated p42/p44 MAPKs (red; c,d,f). (D) Cytoplasmic microinjection of BSA-p90rskwt peptide (a,b) or BSA-p90rskmut peptide (c,d). Indirect immunofluorescence detection was performed as described for C. Véronique Volmat et al. J Cell Sci 2001;114:3433-3443 © The Company of Biologists Limited 2001