Mechanisms of translational control by the 3′ UTR in development and differentiation

Moor, Cornelia H. de; Meijer, Hedda A.; Lissenden, Sarah

doi:10.1016/j.semcdb.2004.11.007

Cited by 293 publications

(237 citation statements)

References 109 publications

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“…MicroRNAs can regulate gene expression by inducing direct cleavage of the targeted mRNAs or inhibiting translation through perfect or nearly perfect complementarity to targeted mRNAs at the 3′-UTRs in animals. 34 The results indicated that miR-181a might regulate the KLF6 expression by cleaving its mRNA. More recently, KLF6 has been reported to be expressed in human umbilical vein ECs and can activate ALK1 gene after wire-induced endothelial denudation.…”

Section: Discussionmentioning

confidence: 96%

MiR-181a Regulates Blood-Tumor Barrier Permeability by Targeting Krüppel-Like Factor 6

Yao

Wang

et al. 2014

J Cereb Blood Flow Metab

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Blood-tumor barrier (BTB) constitutes an efficient organization of tight junctions that impairs the delivery of therapeutic drugs. However, the methods and molecular mechanisms underlying the BTB opening remain elusive. MicroRNAs (miRNAs) have recently emerged as key regulators of various biologic processes and therapeutic targets. In this study, we have identified microRNA-181a (miR-181a) as a critical miRNA in opening BTB. MicroRNA-181a expression was upregulated in glioma endothelial cells (GECs), which were obtained by coculturing endothelial cells (ECs) with glioma cells. Overexpression of miR-181a resulted in an impaired and permeability increased BTB, and meanwhile reduced the expression of zonula occluden (ZO)-1, occludin, and claudin-5. Kruppel-like factor 6 (KLF6), a transcription factor of the zinc-finger family, was downregulated in GECs. Mechanistic investigations defined it as a direct and functional downstream target of miR-181a, which was involved in the regulation of BTB permeability and the expression of ZO-1, occludin, and claudin-5. Furthermore, luciferase assays and chromatin immunoprecipitation assays showed that KLF6 upregulated the promoter activities and interacted with the promoters of ZO-1, occludin, and claudin-5 in GECs. Collectively, we showed the possibility that overexpression of miR-181a contributes to the increased permeability of BTB by targeting KLF6, thereby revealing potential therapeutic targets for the treatment of brain gliomas.

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Section: Discussionmentioning

confidence: 96%

MiR-181a Regulates Blood-Tumor Barrier Permeability by Targeting Krüppel-Like Factor 6

Yao

Wang

et al. 2014

J Cereb Blood Flow Metab

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“…The complete CDS of myostatin has been cloned from swine (Ji et al, 1998), cattle (Grobet et al, 1997), horse (Hosoyama et al, 2002) and sheep (Sharma et al, 1999). MiRNAs negatively regulate gene expression at the posttranscriptional level via binding to the 3'UTR of target mRNAs (Bartel, 2004;Tanzer and Stadler, 2004;de Moor et al, 2005;Gladka et al, 2012). The myostatin 3'UTRs of some species have been known, such as 1552 bp (1262-2814 bp) in goats, 1506 bp (1261-2767 bp) in cattle, 498 bp (1234-1732 bp) in rat (data from GenBank database) and so on.…”

Section: Discussionmentioning

confidence: 99%

“…MicroRNAs are able to suppress translation and/or induce mRNA degradation (Tanzer and Stadler, 2004). Translational control via the 3'UTR can affect formation of the closed loop translation initiation complex, ribosome binding or a post-initiation step (de Moor et al, 2005). The sequence of mature miRNAs are well conserved, whereas the sequence and length of 3'UTR of mRNAs are different among mammalian species (Bartel, 2004).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-27a promotes porcine myoblast proliferation by downregulating myostatin expression

Yang

Chen

Huang

et al. 2014

Animal

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MicroRNAs are endogenous~22nt RNAs that negatively regulate gene expression at the posttranscriptional level via binding to the 3′-untranslated region (3′UTR) of target mRNAs. The microRNA miR-27a was reported to depress the expression of myostatin, a critical inhibitor of skeletal myogenesis, by binding to its 3′UTR in mouse. In this study, we cloned the full-length 3′UTR of porcine myostatin by rapid amplification of 3′-cDNA ends (3′-RACE) and demonstrated that the 3′UTR of porcine myostatin is targeted by miR-27a. The phenomenon that the level of myostatin inversely correlated with miR-27a was observed in fat and heart of pigs and also in proliferating porcine myoblasts. Besides, overexpression of miR-27a in porcine myoblasts promoted cell proliferation by reducing the expression of myostatin. Our data suggest that miR-27a positive regulates porcine myoblast proliferation via targeting myostatin.

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“…In addition, it is known that there are several mechanisms of translational control by the 3 0 UTR. 47 Therefore it is expected that variants in the 3 0 UTR might influence translation and therefore protein levels. Genotype AA in PPP2R1A:c.*465T4A shows a much better lung progression vs genotype TT for the lung function parameter FRC pleth indicating that homozygosity for the mutant allele seems to interfere with translation leading to lower levels of PP2A and therefore to a better residual function of CFTR (Figure 1d).…”

Section: Discussionmentioning

confidence: 99%

Identification of SNPs in the cystic fibrosis interactome influencing pulmonary progression in cystic fibrosis

et al. 2012

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There is growing evidence that the great phenotypic variability in patients with cystic fibrosis (CF) not only depends on the genotype, but apart from a combination of environmental and stochastic factors predominantly also on modifier gene effects. It has been proposed that genes interacting with CF transmembrane conductance regulator (CFTR) and epithelial sodium channel (ENaC) are potential modifiers. Therefore, we assessed the impact of single-nucleotide polymorphisms (SNPs) of several of these interacters on CF disease outcome. SNPs that potentially alter gene function were genotyped in 95 well-characterized p.Phe508del homozygous CF patients. Linear mixed-effect model analysis was used to assess the relationship between sequence variants and the repeated measurements of lung function parameters. In total, we genotyped 72 SNPs in 10 genes. Twenty-five SNPs were used for statistical analysis, where we found strong associations for one SNP in PPP2R4 with the lung clearance index (Pr0.01), the specific effective airway resistance (Pr0.005) and the forced expiratory volume in 1 s (Pr0.005). In addition, we identified one SNP in SNAP23 to be significantly associated with three lung function parameters as well as one SNP in PPP2R1A and three in KRT19 to show a significant influence on one lung function parameter each. Our findings indicate that direct interacters with CFTR, such as SNAP23, PPP2R4 and PPP2R1A, may modify the residual function of p.Phe508del-CFTR while variants in KRT19 may modulate the amount of p.Phe508del-CFTR at the apical membrane and consequently modify CF disease.

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Mechanisms of translational control by the 3′ UTR in development and differentiation

Cited by 293 publications

References 109 publications

MiR-181a Regulates Blood-Tumor Barrier Permeability by Targeting Krüppel-Like Factor 6

MiR-181a Regulates Blood-Tumor Barrier Permeability by Targeting Krüppel-Like Factor 6

MicroRNA-27a promotes porcine myoblast proliferation by downregulating myostatin expression

Identification of SNPs in the cystic fibrosis interactome influencing pulmonary progression in cystic fibrosis

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