Phosphorylation of the chromatin remodeling factor DPF3a induces XXXX through releasing HEY repressors from DNA.

@entity1 @entity712 @entity1184 @entity1283 @entity15774 @entity61403 @entity376 @entity1121 @entity563 @entity472 @entity23423
@entity61403 ( @entity61403 ) is a member of the BAF chromatin remodeling complex. Two isoforms have been described, namely DPF3a and DPF3b. The latter binds to acetylated and methylated @entity376 residues of histones. Here, we elaborate on the role of DPF3a and describe a novel pathway of cardiac gene transcription leading to pathological @entity1283 . Upon @entity1184 stimuli, casein kinase 2 phosphorylates @entity61403 a at @entity563 348. This initiates the interaction of DPF3a with the transcriptional repressors HEY, followed by the release of HEY from the DNA. Moreover, @entity23423 is bound by DPF3a, and is thus recruited to HEY genomic targets upon interaction of the two components. Consequently, the transcription of downstream targets such @entity15774 is initiated and pathological @entity1283 is established. In @entity1 , @entity61403 a is significantly up-regulated in @entity1184 hearts of @entity1 with @entity1121 or @entity472 . Taken together, we show that activation of DPF3a upon @entity1184 stimuli switches cardiac fetal gene expression from being silenced by HEY to being activated by @entity23423 . Thus, we present a novel pathway for pathological @entity1283 , whose inhibition is a long-term therapeutic goal for the treatment of the course of @entity712 .
