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Nη-Substituted Arginyl Peptide Inhibitors of Protein Arginine N-Methyltransferases
Journal article   Open access   Peer reviewed

Nη-Substituted Arginyl Peptide Inhibitors of Protein Arginine N-Methyltransferases

Ted M Lakowski, Peter ’t Hart, Christopher A Ahern, Nathaniel I Martin and Adam Frankel
ACS chemical biology, Vol.5(11), pp.1053-1063
11/19/2010
DOI: 10.1021/cb100161u
PMID: 20701328
url
https://dspace.library.uu.nl/handle/1874/395680View
Open Access

Abstract

Protein arginine N-methyltransferases (PRMTs) catalyze the post-translational methylation of arginine residues within substrate proteins. Their roles in the epigenetic regulation of gene expression make them viable targets for drug discovery. Peptides containing a single arginine residue substituted at the guanidino nitrogen (N(η)) with an ethyl group bearing zero to three fluorine atoms (R1-1, -2, -3, and -4) have been synthesized and tested for methylation and inhibition activity with PRMT1, PRMT6, and CARM1. Only the nonfluorinated R1-1 peptide is methylated by PRMT1, demonstrating that the N(η)-substituted arginine is accommodated by its active site. The R1-1 ethyl-substituted guanidine N(η) was further identified as the methylation site via mass spectrometry. Although weak inhibitors of CARM1, R1-1, -2, -3, and -4 are potent inhibitors of PRMT1 and PRMT6. These peptides are more potent against PRMT1 than product inhibitor peptides, showing that N(η)-substituted arginyl peptides do not work by a purely product inhibitor mechanism. A trend of increasing potency with an increase in the number of fluorine atoms is observed for PRMT1, which may result from the corresponding change in the guanidino dipole moment. Modeling of the ethyl-arginine moiety of the R1-1 peptide demonstrates that the active site of PRMT1 accommodates such modifications. N(η)-Substituted arginyl peptides represent lead compounds for the further development of inhibitors that target the methyl-acceptor binding site of PRMTs.

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