Amyloid precursor protein regulates neurogenesis by antagonizing miR-574-5p in the developing cerebral cortex

Zhang, Wei; Selvaratnam, Thevapriya; Kim, Paul J.; Yu, Weiping; Je, H. Shawn; Tan, Eng King; Zeng, Li

doi:10.1038/ncomms4330

Cited by 55 publications

(72 citation statements)

References 37 publications

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“…4d). We note that the presence of a PHE signal in the p-doped region can be explained by the existence of Rashba-type bands in the hybridized SSs and/or bulk valence bands [14] since the relative position of the CNP is close to the maximum of the bulk valence bands [18,55,56]. In our experiment, the PHE is not observed in the n-type region of 3QL heterostructures.…”

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Unconventional planar Hall effect in exchange-coupled topological insulator–ferromagnetic insulator heterostructures

et al. 2018

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The Dirac electrons occupying the surface states (SSs) of topological insulators (TIs) have been predicted to exhibit many exciting magneto-transport phenomena. Here we report on the first experimental observation of an unconventional planarHall effect (PHE) and an electrically gate-tunable hysteretic planar magnetoresistance (PMR) in EuS/TI heterostructures, in which EuS is a ferromagnetic insulator (FMI) with an in-plane magnetization. In such exchangecoupled FMI/TI heterostructures, we find a significant (suppressed) PHE when the in-plane magnetic field is parallel (perpendicular) to the electric current. This

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“…was controlled to locate the chemical potential close to the Dirac point in order to enhance the contribution of the SSs in magneto-transport [16,[18][19][20]. The growth was monitored using in-situ reflective high-energy electron diffraction (RHEED).…”

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confidence: 99%

Unconventional planar Hall effect in exchange-coupled topological insulator–ferromagnetic insulator heterostructures

et al. 2018

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“…We also identified 6 additional miRNAs (miR-574-5p, miR-3659, miR-1236-5p, miR-4481, miR-4745-5p and miR-4765) that possessed 5 complementary nucleotides in both site I and II but matched the other search criteria (S3A Fig). Among these miRNAs, we focused on 3 candidates: miR-504-3p, due to its high similarity to miR-122; miR-574-5p, because it has been reported to play a functional role in neuronal cells [33, 34]; miR-1236-5p, because it has substantial expression in several tissues [34]. The tissue specificity index (TSI) can be used classify miRNAs as tissue-specific (TSI>0.85) or housekeeping (TSI<0.5) based on the expression pattern [34].…”

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confidence: 99%

Various miRNAs are involved in efficient HCV replication

Ono

Fukuhara

et al. 2020

Preprint

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17One of the determinants for tissue tropism of hepatitis C virus (HCV) is miR-122, a liver-specific 18 microRNA. Recently, it has been reported that interaction of miR-122 to HCV RNA induces a 19 conformational change of the 5'UTR internal ribosome entry site (IRES) structure to form stem-loop II 20 structure (SLII) and hijack of translating 80S ribosome through the binding of SLIII to 40S subunit, 21 which leads to efficient translation. On the other hand, low levels of HCV-RNA replication have also 22 45 3 both G28 and C29 in the 5'UTR. The interaction of these non-hepatic miRNAs with the 5'UTR can 46 facilitate not only the folding of active HCV IRES but also the stabilization of IRES 3D structure in 47 order to facilitate binding to the ribosome. These results suggest the possibility of replication of HCV in 48 non-hepatic cells through interaction with miRNAs other than miR-122 and provide insight into the 49 establishment of persistent infection of HCV in non-hepatic tissues that lead to the development of 50 extrahepatic manifestations. 51 52

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“…1c). miR-574-5p has been identified as an oncogenic miRNA 45 and is involved in neurogenesis 46 . miR-574-3p is recognized as an antitumor miRNA 47,48 .…”

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confidence: 99%

MicroRNA-574 Regulates FAM210A Expression and Influences Pathological Cardiac Remodeling

Subbaiah

Jiang

et al. 2020

Preprint

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Aberrant synthesis of mitochondrial proteins impairs cardiac function and causes heart disease. However, the mechanism of regulation of mitochondria encoded protein expression during cardiac disease remains underexplored. Here, we have shown that multiple pathogenic cardiac stressors induce the expression of miR-574 guide and passenger strands (miR-574-5p/3p) in both humans and mice. miR-574 knockout mice exhibit severe cardiac disorder under heart disease-triggering stresses. miR-574-5p/3p mimics that are delivered systematically using nanoparticles reduce cardiac pathogenesis under disease insults.Transcriptome analysis of miR-574-null hearts uncovers FAM210A as a common target mRNA for both strands of miR-574. The interactome capture and translational state analyses suggest that FAM210A interacts with mitochondrial translation factors and regulates the protein expression of mitochondrial encoded electron transport chain genes. Using a human cardiomyocyte cell culture system, we discover that miR-574 regulates FAM210A expression and modulates mitochondrial encoded protein expression, which influences cardiac remodeling in heart failure.Abbreviations of key terms: ACM, adult cardiomyocytes; CF, cardiac fibroblasts; CM, cardiomyocytes; ETC, electron transport chain; FAM210A, family with sequence similarity 210 member A; HF, heart failure; ISO, isoproterenol; MEG, mitochondrial encoded gene; MI, myocardial infarction; NEMG, nuclear-encoded mitochondrial gene; RBP, RNA-binding protein; RISC, RNA-induced silencing complex; TAC, transverse aortic constriction; UTR, untranslated region Results Cardiac stress induces miR-574-5p and miR-574-3p in human and mouse heartsFrom data mining of unbiased screening data from four laboratories, the guide strand miR-574-5p has been identified as a miRNA that is robustly induced in the heart in response to pathological cardiac remodeling, which included the cardiac tissues of patients during the initial stages following MI onset 33 , a mouse model of left coronary artery occlusion-derived MI 24 , and aged murine hearts ( Fig. 1a) 26 . On the other hand, the passenger strand miR-574-3p is increased in the human hearts after MI and more remarkably induced by exercise training in murine hearts 34 . The cardiac functions of complementary strands of miR-574-5p and miR-574-3p remain unknown. miR-574 is conserved in 43 animal species (10 primates and 33 mammals, UCSC Genome Browser). In mammals, miR-574 is located in intron 1 of the host gene FAM114A1 (Family with sequence similarity 114 member A1) ( Fig. 1b). We confirmed that both miR-574-5p and miR-574-3p were significantly induced in heart tissues of chronic HF patients, with the expression level of miR-574-5p even higher than that of miR-574-3p (Fig. 1c). Northern blot analysis showed that both miR-574-5p and miR-574-3p were expressed in the normal murine heart ( Supplementary Fig. 1a). miR-574-5p and miR-574-3p were both significantly induced in isoproterenol (ISO)-or transverse aortic constriction (TAC)-treated mouse hearts, compar...

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Amyloid precursor protein regulates neurogenesis by antagonizing miR-574-5p in the developing cerebral cortex

Cited by 55 publications

References 37 publications

Unconventional planar Hall effect in exchange-coupled topological insulator–ferromagnetic insulator heterostructures

Unconventional planar Hall effect in exchange-coupled topological insulator–ferromagnetic insulator heterostructures

Various miRNAs are involved in efficient HCV replication

MicroRNA-574 Regulates FAM210A Expression and Influences Pathological Cardiac Remodeling

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