Erratum: Corrigendum: A brain-specific microRNA regulates dendritic spine development

Schratt, Gerhard; Tuebing, Fabian; Nigh, Elizabeth A.; Kane, Christina G.; Sabatini, Mary E.; Kiebler, Michael A.; Greenberg, Michael E.

doi:10.1038/nature04909

Cited by 10 publications

(5 citation statements)

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“…Moreover, that the derepression is accompanied by the release of CAT-1 mRNA from cytoplasmic processing bodies and its entry into polysomes and that the process involves binding of HuR, trans -acting AU rich element (ARE) binding protein, to the 3'UTR of CAT-1 mRNA [31]. There is also additional evidence indicating that some miRNA-controlled mRNAs can be relieved from repression by synaptic stimulation [32,33] indicating that miRNA regulation is more pronounced than previously anticipated and that it is able to respond quickly to specific cellular needs. What is yet to be determined is whether changes in oxygen tension provide a like mechanism for derepression of miRNAs against HMGA2.…”

Section: Resultsmentioning

confidence: 99%

High mobility group A2 is a target for miRNA-98 in head and neck squamous cell carcinoma

et al. 2007

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Background: HMGA2 expression has been shown to be associated with enhanced selective chemosensitivity towards the topoisomerase (topo) II inhibitor, doxorubicin, in cancer cells. Although the roles of signaling cascades and proteins as regulatory factors in development, neoplasia and adaptation to the environment are becoming well established, evidence for the involvement of regulatory small RNA molecules, such as microRNAs (miRNAs) as important regulators of both transcriptional and posttranscriptional gene silencing is presently mounting.

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Section: Resultsmentioning

confidence: 99%

High mobility group A2 is a target for miRNA-98 in head and neck squamous cell carcinoma

et al. 2007

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“…When activated, LIMK induces actin polymerization through the phosphorylation of cofilin. Specifically, in its unphosphorylated state, cofilin depolymerizes actin, but its depolymerizing activity is inhibited when it is phosphorylated by LIMK [23,[33][34][35]. Indeed, Rac1/PAK-and RhoA/ROCK-induced cofilin reorganization of actin can be blocked by LIMK inhibition [36,37].…”

Section: Introductionmentioning

confidence: 99%

Effects of Hippocampal LIMK Inhibition on Memory Acquisition, Consolidation, Retrieval, Reconsolidation, and Extinction

et al. 2017

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Long-lasting changes in dendritic spines provide a physical correlate for memory formation and persistence. LIM kinase (LIMK) plays a critical role in orchestrating dendritic actin dynamics during memory processing, since it is the convergent downstream target of both the Rac1/PAK and RhoA/ROCK pathways that in turn induce cofilin phosphorylation and prevent depolymerization of actin filaments. Here, using a potent LIMK inhibitor (BMS-5), we investigated the role of LIMK activity in the dorsal hippocampus during contextual fear memory in rats. We first found that post-training administration of BMS-5 impaired memory consolidation in a dose-dependent manner. Inhibiting LIMK before training also disrupted memory acquisition. We then demonstrated that hippocampal LIMK activity seems to be critical for memory retrieval and reconsolidation, since both processes were impaired by BMS-5 treatment. Contextual fear memory extinction, however, was not sensitive to the same treatment. In conclusion, our findings demonstrate that hippocampal LIMK activity plays an important role in memory acquisition, consolidation, retrieval, and reconsolidation during contextual fear conditioning.

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“…In other cases, miRNAs expression was restricted to highly specialized compartments. For example, miR-134 is involved in the regulation of the size of the dendritic spine size by locally inhibiting LIMK1 (LIM domain Kinase 1), a kinase responsible of actin polymerization [77].…”

Section: Biogenesis and Regulatory Functionsmentioning

confidence: 99%

miRNAs as Influencers of Cell–Cell Communication in Tumor Microenvironment

Conti

Varano

Simioni

et al. 2020

Cells

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microRNAs (miRNAs) are small noncoding RNAs that regulate gene expression at the posttranscriptional level, inducing the degradation of the target mRNA or translational repression. MiRNAs are involved in the control of a multiplicity of biological processes, and their absence or altered expression has been associated with a variety of human diseases, including cancer. Recently, extracellular miRNAs (ECmiRNAs) have been described as mediators of intercellular communication in multiple contexts, including tumor microenvironment. Cancer cells cooperate with stromal cells and elements of the extracellular matrix (ECM) to establish a comfortable niche to grow, to evade the immune system, and to expand. Within the tumor microenvironment, cells release ECmiRNAs and other factors in order to influence and hijack the physiological processes of surrounding cells, fostering tumor progression. Here, we discuss the role of miRNAs in the pathogenesis of multicomplex diseases, such as Alzheimer’s disease, obesity, and cancer, focusing on the contribution of both intracellular miRNAs, and of released ECmiRNAs in the establishment and development of cancer niche. We also review growing evidence suggesting the use of miRNAs as novel targets or potential tools for therapeutic applications.

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Erratum: Corrigendum: A brain-specific microRNA regulates dendritic spine development

Cited by 10 publications

References 1 publication

High mobility group A2 is a target for miRNA-98 in head and neck squamous cell carcinoma

High mobility group A2 is a target for miRNA-98 in head and neck squamous cell carcinoma

Effects of Hippocampal LIMK Inhibition on Memory Acquisition, Consolidation, Retrieval, Reconsolidation, and Extinction

miRNAs as Influencers of Cell–Cell Communication in Tumor Microenvironment

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