In previous reports, we described the functional properties of ZNF224, a member of the KRAB-ZFP
family. We demonstrated that ZNF224-mediated repression requires the recruitment of KAP1 and of
the histone deacetylase HDAC1, in order to inhibit the human aldolase A gene transcription [10].
Moreover, we identified PRMT5, a type II protein arginine methyltransferase as a novel component of
ZNF224 transcriptional repression complex and demonstrated that histone arginine methylation by
PRMT5 is necessary for ZNF224-mediated gene repression [11].
These findings prompted us to explore the possibility that PRMT5 interacts with KAP1 and the role
of PRMT5 on KAP1 methylation.