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Overexpression of miR-128 specifically inhibits the truncated isoform of NTRK3 and upregulates BCL2 in SH-SY5Y neuroblastoma cells

机译:miR-128的过表达特异性抑制NTRK3的截短亚型并上调SH-SY5Y神经母细胞瘤细胞中的BCL2

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摘要

BackgroundNeurotrophins and their receptors are key molecules in the regulation of neuronal differentiation and survival. They mediate the survival of neurons during development and adulthood and are implicated in synaptic plasticity. The human neurotrophin-3 receptor gene NTRK3 yields two major isoforms, a full-length kinase-active form and a truncated non-catalytic form, which activates a specific pathway affecting membrane remodeling and cytoskeletal reorganization. The two variants present non-overlapping 3'UTRs, indicating that they might be differentially regulated at the post-transcriptional level. Here, we provide evidence that the two isoforms of NTRK3 are targeted by different sets of microRNAs, small non-coding RNAs that play an important regulatory role in the nervous system.
机译:背景神经营养蛋白及其受体是调节神经元分化和存活的关键分子。它们在发育和成年期间介导神经元的存活,并牵涉突触可塑性。人Neurotrophin-3受体基因NTRK3产生两种主要的同工型,即全长激酶活性型和截短的非催化型,后者激活了影响膜重塑和细胞骨架重组的特定途径。这两个变体呈现不重叠的3'UTR,表明它们可能在转录后水平上受到差异调节。在这里,我们提供的证据表明,NTRK3的两个同工型分别被不同的microRNA组靶向,微小的非编码RNA在神经系统中起着重要的调节作用。

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