@article{Rehfeld_Maticzka_Grosser-The_RNA_prote-2018,
author = {Rehfeld, Frederick and Maticzka, Daniel and Grosser, Sabine 
          and Knauff, Pina and Eravci, Murat and Vida, Imre and 
          Backofen, Rolf and Wulczyn, F. Gregory},
title = {The {RNA}-binding protein {ARPP21} controls dendritic 
         branching by functionally opposing the {miRNA} it hosts},
journal = {Nat Commun},
year = {2018},
doi = {10.1038/s41467-018-03681-3},
volume = {9},
user = {maticzkd},
pmid = {29581509},
pages = {1235},
number = {1},
issn = {2041-1723},
abstract = {About half of mammalian miRNA genes lie within introns of 
            protein-coding genes, yet little is known about functional 
            interactions between miRNAs and their host genes. The 
            intronic miRNA miR-128 regulates neuronal excitability and 
            dendritic morphology of principal neurons during mouse 
            cerebral cortex development. Its conserved host genes, 
            R3hdm1 and Arpp21, are predicted RNA-binding proteins. Here 
            we use iCLIP to characterize ARPP21 recognition of 
            uridine-rich sequences with high specificity for 3'UTRs. 
            ARPP21 antagonizes miR-128 activity by co-regulating a 
            subset of miR-128 target mRNAs enriched for 
            neurodevelopmental functions. Protein-protein interaction 
            data and functional assays suggest that ARPP21 acts as a 
            positive post-transcriptional regulator by interacting with 
            the translation initiation complex eIF4F. This molecular 
            antagonism is reflected in inverse activities during 
            dendritogenesis: miR-128 overexpression or knockdown of 
            ARPP21 reduces dendritic complexity; ectopic ARPP21 leads to 
            an increase. Thus, we describe a unique example of 
            convergent function by two products of a single gene.}
}