324 results found
    1. Neuroscience

    MicroRNA-9 controls dendritic development by targeting REST

    Sebastian A Giusti, Annette M Vogl ... Damian Refojo
    Conditional transgenic miR-9 sponge mice exhibit developmental defects in dendrite growth due to up-regulation of the transcriptional repressor REST.
    1. Developmental Biology
    2. Neuroscience

    Ngn1 inhibits astrogliogenesis through induction of miR-9 during neuronal fate specification

    Jing Zhao, Quan Lin ... Yi Sun
    During neurogenesis, Neurogenin 1 activates the microRNA miR-9, which directly targets the Jak-Stat pathway to inhibit astrogliogenesis.
    1. Neuroscience

    miR-9 regulates basal ganglia-dependent developmental vocal learning and adult vocal performance in songbirds

    Zhimin Shi, Zoe Piccus ... XiaoChing Li
    Gene manipulation combined with behavior analysis reveals a role of miR-9 in modulating basal-ganglia-dependent developmental vocal learning and adult vocal performance via regulating the FOXP1/FOXP2 gene network and dopamine signaling in songbirds.
    1. Cell Biology
    2. Stem Cells and Regenerative Medicine

    Mir155 regulates osteogenesis and bone mass phenotype via targeting S1pr1 gene

    Zhichao Zheng, Lihong Wu ... Janak L Pathak
    Mir155 showed a catabolic effect on osteogenesis and bone mass phenotype via interaction with the S1pr1 gene, suggesting inhibition of Mir155 as a potential approach to bone regeneration and bone defect healing.
    1. Stem Cells and Regenerative Medicine

    Stress responsive miR-31 is a major modulator of mouse intestinal stem cells during regeneration and tumorigenesis

    Yuhua Tian, Xianghui Ma ... Zhengquan Yu
    miR-31 drives proliferation of intestinal stem cells, and protects intestinal stem cells against apoptosis both during homeostasis and regeneration in response to ionizing radiation injury, and promotes intestinal tumorigenesis through regulation of multiple signaling pathways.
    1. Genetics and Genomics

    miR-1 coordinately regulates lysosomal v-ATPase and biogenesis to impact proteotoxicity and muscle function during aging

    Isabelle Schiffer, Birgit Gerisch ... Adam Antebi
    Coordinate control of lysosomal v-ATPase subunits and biogenesis factor TFEB by miR-1 identifies a key regulatory axis with strong links to age-related proteotoxic disease.
    1. Neuroscience

    Learning induces the translin/trax RNase complex to express activin receptors for persistent memory

    Alan Jung Park, Robbert Havekes ... Ted Abel
    Combination of in vitro and in vivo approaches reveal how learning suppresses the microRNA system to trigger de novo synthesis of plasticity proteins, a missing link in the current model of microRNA-mediated translation in persistent synaptic plasticity and memory.
    1. Developmental Biology
    2. Genetics and Genomics

    Feedback between a retinoid-related nuclear receptor and the let-7 microRNAs controls the pace and number of molting cycles in C. elegans

    Ruhi Patel, Himani Galagali ... Alison R Frand
    A genetic oscillator composed of NHR-23 and let-7 family of microRNAs links the molting cycle timer and the heterochronic pathway to regulate the pace of molting in C. elegans and ensure that worms molt only four times.
    1. Developmental Biology

    MicroRNA-934 is a novel primate-specific small non-coding RNA with neurogenic function during early development

    Kanella Prodromidou, Ioannis S Vlachos ... Rebecca Matsas
    Primate-specific miR-934 mediates neurogenesis and downstream neuronal differentiation processes, modulating the expression of genes associated with the subplate, a region most prominent in primates, emerging during early cortical development.
    1. Cancer Biology

    Inactivation of oncogenic cAMP-specific phosphodiesterase 4D by miR-139-5p in response to p53 activation

    Bo Cao, Kebing Wang ... Hua Lu
    The tumor suppressor p53 prevents tumor cell growth by employing a small RNA called miR-139-5p to inhibit the activity of an tumorigenic protein, cAMP-specific phosphodiesterase 4D.

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