RNA-binding protein that inhibits processing of pre-let-7miRNAs and regulates translation of mRNAs that control developmentaltiming, pluripotency and metabolism. Seems torecognize a common structural G-quartet (G4) feature in its miRNA andmRNA targets. 'Translational enhancer' that drives specificmRNAs to polysomes and increases the efficiency of protein synthesis. Its association with the translational machinery and target mRNAsresults in an increased number of initiation events per molecule ofmRNA and, indirectly, in mRNA stabilization. Binds IGF2 mRNA, MYOD1mRNA, ARBP/36B4 ribosomal protein mRNA and its own mRNA. Essential forskeletal muscle differentiation program through the translational up-regulation of IGF2 expression. Suppressor of microRNA (miRNA) biogenesis, including that of let-7, miR107, miR-143 and miR-200c. Specifically binds the miRNA precursors (pre-miRNAs), recognizing an5'-GGAG-3' motif found in pre-miRNA terminal loop, and recruits TUT4and TUT7 uridylyltransferases. This results in the terminaluridylation of target pre-miRNAs. Uridylated pre-miRNAs fail to beprocessed by Dicer and undergo degradation. The repression of let-7expression is required for normal development and contributes tomaintain the pluripotent state by preventing let-7-mediateddifferentiation of embryonic stem cells. Localized to theperiendoplasmic reticulum area, binds to a large number of splicedmRNAs and inhibits the translation of mRNAs destined for the ER, reducing the synthesis of transmembrane proteins, ER or Golgi lumenproteins, and secretory proteins. Binds to and enhances the translationof mRNAs for several metabolic enzymes, such as PFKP, PDHA1 or SDHA, increasing glycolysis and oxidative phosphorylation. Which, with thelet-7 repression may enhance tissue repair in adult tissue. [1-5]

MGSVSNQQFAGGCAKAAEEAPEEAPEDAARAADEPQLLHGAGICKWFNVRMGFGFLSMTARAGVALDPPVDVFVHQSKLHMEGFRSLKEGEAVEFTFKKSAKGLESIRVTGPGGVFCIGSERRPKGKSMQKRRSKGDRCYNCGGLDHHAKECKLPPQPKKCHFCQSISHMVASCPLKAQQGPSAQGKPTYFREEEEEIHSPTLLPEAQN