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Relevant bibliographies by topics / Translational silencing

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Academic literature on the topic 'Translational silencing'

Author: Grafiati

Published: 28 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Translational silencing"

1

Sampath, Prabha, Barsanjit Mazumder, Vasudevan Seshadri, and Paul L. Fox. "Transcript-Selective Translational Silencing by Gamma Interferon Is Directed by a Novel Structural Element in the Ceruloplasmin mRNA 3′ Untranslated Region." Molecular and Cellular Biology 23, no. 5 (March 1, 2003): 1509–19. http://dx.doi.org/10.1128/mcb.23.5.1509-1519.2003.

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ABSTRACT Transcript-selective translational control of eukaryotic gene expression is often directed by a structural element in the 3′ untranslated region (3′-UTR) of the mRNA. In the case of ceruloplasmin (Cp), induced synthesis of the protein by gamma interferon (IFN-γ) in U937 monocytic cells is halted by a delayed translational silencing mechanism requiring the binding of a cytosolic inhibitor to the Cp 3′-UTR. Silencing requires the essential elements of mRNA circularization, i.e., eukaryotic initiation factor 4G, poly(A)-binding protein, and poly(A) tail. We here determined the minimal silencing element in the Cp 3′-UTR by progressive deletions from both termini. A minimal, 29-nucleotide (nt) element was determined by gel shift assay to be sufficient for maximal binding of the IFN-γ-activated inhibitor of translation (GAIT), an as-yet-unidentified protein or complex. The interaction was shown to be functional by an in vitro translation assay in which the GAIT element was used as a decoy to overcome translational silencing. Mutation analysis showed that the GAIT element contained a 5-nt terminal loop, a weak 3-bp helix, an asymmetric internal bulge, and a proximal 6-bp helical stem. Two invariant loop residues essential for binding activity were identified. Ligation of the GAIT element immediately downstream of a luciferase reporter conferred the translational silencing response to the heterologous transcript in vitro and in vivo; a construct containing a nonbinding, mutated GAIT element was ineffective. Translational silencing of Cp, and possibly other transcripts, mediated by the GAIT element may contribute to the resolution of the local inflammatory response following cytokine activation of macrophages.

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Baez, María Verónica, Luciana Luchelli, Darío Maschi, Martín Habif, Malena Pascual, María Gabriela Thomas, and Graciela Lidia Boccaccio. "Smaug1 mRNA-silencing foci respond to NMDA and modulate synapse formation." Journal of Cell Biology 195, no. 7 (December 26, 2011): 1141–57. http://dx.doi.org/10.1083/jcb.201108159.

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Mammalian Smaug1/Samd4A is a translational repressor. Here we show that Smaug1 forms mRNA-silencing foci located at postsynapses of hippocampal neurons. These structures, which we have named S-foci, are distinct from P-bodies, stress granules, or other neuronal RNA granules hitherto described, and are the first described mRNA-silencing foci specific to neurons. RNA binding was not required for aggregation, which indicates that S-foci formation is not a consequence of mRNA silencing. N-methyl-d-aspartic acid (NMDA) receptor stimulation provoked a rapid and reversible disassembly of S-foci, transiently releasing transcripts (the CaMKIIα mRNA among others) to allow their translation. Simultaneously, NMDA triggered global translational silencing, which suggests the specific activation of Smaug1-repressed transcripts. Smaug1 is expressed during synaptogenesis, and Smaug1 knockdown affected the number and size of synapses, and also provoked an impaired response to repetitive depolarizing stimuli, as indicated by a reduced induction of Arc/Arg3.1. Our results suggest that S-foci control local translation, specifically responding to NMDA receptor stimulation and affecting synaptic plasticity.

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Mazumder, Barsanjit, Vasudevan Seshadri, Hiroaki Imataka, Nahum Sonenberg, and Paul L. Fox. "Translational Silencing of Ceruloplasmin Requires the Essential Elements of mRNA Circularization: Poly(A) Tail, Poly(A)-Binding Protein, and Eukaryotic Translation Initiation Factor 4G." Molecular and Cellular Biology 21, no. 19 (October 1, 2001): 6440–49. http://dx.doi.org/10.1128/mcb.21.19.6440-6449.2001.

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ABSTRACT Ceruloplasmin (Cp) is a glycoprotein secreted by the liver and monocytic cells and probably plays roles in inflammation and iron metabolism. We showed previously that gamma interferon (IFN-γ) induced Cp synthesis by human U937 monocytic cells but that the synthesis was subsequently halted by a transcript-specific translational silencing mechanism involving the binding of a cytosolic factor(s) to the Cp mRNA 3′ untranslated region (UTR). To investigate how protein interactions at the Cp 3′-UTR inhibit translation initiation at the distant 5′ end, we considered the “closed-loop” model of mRNA translation. In this model, the transcript termini are brought together by interactions of poly(A)-binding protein (PABP) with both the poly(A) tail and initiation factor eIF4G. The effect of these elements on Cp translational control was tested using chimeric reporter transcripts in rabbit reticulocyte lysates. The requirement for poly(A) was shown since the cytosolic inhibitor from IFN-γ-treated cells minimally inhibited the translation of a luciferase reporter upstream of the Cp 3′-UTR but almost completely blocked the translation of a transcript containing a poly(A) tail. Likewise, a requirement for poly(A) was shown for silencing of endogenous Cp mRNA. We considered the possibility that the cytosolic inhibitor blocked the interaction of PABP with the poly(A) tail or with eIF4G. We found that neither of these interactions were inhibited, as shown by immunoprecipitation of PABP followed by quantitation of the poly(A) tail by reverse transcription-PCR and of eIF4G by immunoblot analysis. We considered the alternate possibility that these interactions were required for translational silencing. When PABP was depleted from the reticulocyte lysate with anti-human PABP antibody, the cytosolic factor did not inhibit translation of the chimeric reporter, thus showing the requirement for PABP. Similarly, in lysates treated with anti-human eIF4G antibody, the cytosolic extract did not inhibit the translation of the chimeric reporter, thereby showing a requirement for eIF4G. These data show that translational silencing of Cp requires interactions of three essential elements of mRNA circularization, poly(A), PABP, and eIF4G. We suggest that Cp mRNA circularization brings the cytosolic Cp 3′-UTR-binding factor into the proximity of the translation initiation site, where it silences translation by an undetermined mechanism. These results suggest that in addition to its important function in increasing the efficiency of translation, transcript circularization may serve as an essential structural determinant for transcript-specific translational control.

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4

Nair, Asha P. K., Hans H. Hirsch, Marco Colombi, and Christoph Moroni. "Cyclosporin A Promotes Translational Silencing of Autocrine Interleukin-3 via Ribosome-Associated Deadenylation." Molecular and Cellular Biology 19, no. 1 (January 1, 1999): 889–98. http://dx.doi.org/10.1128/mcb.19.1.889.

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ABSTRACT Translation is regulated predominantly by an interplay betweencis elements at the 3′ and 5′ ends of mRNAs andtrans-acting proteins. Cyclosporin A (CsA), a calcineurin antagonist and blocker of interleukin-2 (IL-2) transcription in T cells, was found to inhibit translation of IL-3 mRNA in autocrine mast cell tumor lines. The mechanism involved ribosome-associated poly(A) shortening and required an intact AU-rich element in the 3′ untranslated region. FK506, another calcineurin inhibitor, shared the effect. The translational inhibition by CsA was specific to oncogenically induced lymphokines IL-3 and IL-4 but not to IL-6, c-jun, and c-myc, which are expressed in the nonmalignant precursor cells. Furthermore, no translational down-regulation of the mRNA was observed in IL-3-transfected precursor cells. These data suggest that translational silencing is associated with the tumor phenotype.

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Chapat, Clément, Seyed Mehdi Jafarnejad, Edna Matta-Camacho, Geoffrey G. Hesketh, Idit A. Gelbart, Jan Attig, Christos G. Gkogkas, et al. "Cap-binding protein 4EHP effects translation silencing by microRNAs." Proceedings of the National Academy of Sciences 114, no. 21 (May 9, 2017): 5425–30. http://dx.doi.org/10.1073/pnas.1701488114.

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MicroRNAs (miRNAs) play critical roles in a broad variety of biological processes by inhibiting translation initiation and by destabilizing target mRNAs. The CCR4–NOT complex effects miRNA-mediated silencing, at least in part through interactions with 4E-T (eIF4E transporter) protein, but the precise mechanism is unknown. Here we show that the cap-binding eIF4E-homologous protein 4EHP is an integral component of the miRNA-mediated silencing machinery. We demonstrate that the cap-binding activity of 4EHP contributes to the translational silencing by miRNAs through the CCR4–NOT complex. Our results show that 4EHP competes with eIF4E for binding to 4E-T, and this interaction increases the affinity of 4EHP for the cap. We propose a model wherein the 4E-T/4EHP interaction engenders a closed-loop mRNA conformation that blocks translational initiation of miRNA targets.

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Huarte, Joaquin, André Stutz, Marcia L. O'Connell, Pascale Gubler, Dominique Belin, Andrew L. Darrow, Sidney Strickland, and Jean-Dominique Vassalli. "Transient translational silencing by reversible mRNA deadenylation." Cell 69, no. 6 (June 1992): 1021–30. http://dx.doi.org/10.1016/0092-8674(92)90620-r.

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7

Vyas, Keyur, Sujan Chaudhuri, Douglas W. Leaman, Anton A. Komar, Alla Musiyenko, Sailen Barik, and Barsanjit Mazumder. "Genome-Wide Polysome Profiling Reveals an Inflammation-Responsive Posttranscriptional Operon in Gamma Interferon-Activated Monocytes." Molecular and Cellular Biology 29, no. 2 (November 10, 2008): 458–70. http://dx.doi.org/10.1128/mcb.00824-08.

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ABSTRACT We previously showed that ribosomal protein L13a is required for translational silencing of gamma interferon (IFN-γ)-induced ceruloplasmin (Cp) synthesis in monocytes. This silencing also requires the presence of the GAIT (IFN-gamma activated inhibitor of translation) element in the 3′ untranslated region (UTR) of Cp mRNA. Considering that Cp is an inflammatory protein, we hypothesized that this mechanism may have evolved to silence a family of proinflammatory proteins, of which Cp is just one member. To identify the other mRNAs that are targets for this silencing, we performed a genome-wide analysis of the polysome-profiled mRNAs by using an Affymetrix GeneChip and an inflammation-responsive gene array. A cluster of mRNAs encoding different chemokines and their receptors was identified as common hits in the two approaches and validated by real-time PCR. In silico predicted GAIT hairpins in the 3′ UTRs of the target mRNAs were confirmed as functional cis-acting elements for translational silencing by luciferase reporter assays. Consistent with Cp, the newly identified target mRNAs also required L13a for silencing. Our studies have identified a new inflammation-responsive posttranscriptional operon that can be regulated directly at the level of translation in IFN-γ-activated monocytes. This regulation of a cohort of mRNAs encoding inflammatory proteins may be important to resolve inflammation.

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Stutz, A., J. Huarte, P. Gubler, B. Conne, D. Belin, and J. D. Vassalli. "In vivo antisense oligodeoxynucleotide mapping reveals masked regulatory elements in an mRNA dormant in mouse oocytes." Molecular and Cellular Biology 17, no. 4 (April 1997): 1759–67. http://dx.doi.org/10.1128/mcb.17.4.1759.

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In mouse oocytes, tissue-type plasminogen activator (tPA) mRNA is under translational control. The newly transcribed mRNA undergoes deadenylation and translational silencing in growing oocytes, while readenylation and translation occur during meiotic maturation. To localize regulatory elements controlling tPA mRNA expression, we identified regions of the endogenous transcript protected from hybridization with injected antisense oligodeoxynucleotides. Most of the targeted sequences in either the 5' untranslated region (5'UTR), coding region, or 3'UTR were accessible to hybridization, as revealed by inhibition of tPA synthesis and by RNase protection. Two protected regions were identified in the 3'UTR of tPA mRNA in primary oocytes: the adenylation control element (ACE) and the AAUAAA polyadenylation signal. These sequences were previously shown to be involved in the translational control of injected reporter transcripts. During the first hour of meiotic maturation, part of the ACE and the AAUAAA hexanucleotide became accessible to hybridization, suggesting a partial unmasking of the 3'UTR of this mRNA before it becomes translationally competent. Our results demonstrate that in vivo antisense oligodeoxynucleotide mapping can reveal the dynamics of regulatory features of a native mRNA in the context of the intact cell. They suggest that specific regions in the 3'UTR of tPA mRNA function as cis-acting masking determinants involved in the silencing of tPA mRNA in primary oocytes.

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Ostareck-Lederer, Antje, Dirk H. Ostareck, Christophe Cans, Gitte Neubauer, Karol Bomsztyk, Giulio Superti-Furga, and Matthias W. Hentze. "c-Src-Mediated Phosphorylation of hnRNP K Drives Translational Activation of Specifically Silenced mRNAs." Molecular and Cellular Biology 22, no. 13 (July 1, 2002): 4535–43. http://dx.doi.org/10.1128/mcb.22.13.4535-4543.2002.

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ABSTRACT hnRNPK and hnRNP E1/E2 mediate translational silencing of cellular and viral mRNAs in a differentiation-dependent way by binding to specific regulatory sequences. The translation of 15-lipoxygenase (LOX) mRNA in erythroid precursor cells and of the L2 mRNA of human papilloma virus type 16 (HPV-16) in squamous epithelial cells is silenced when either of these cells is immature and is activated in maturing cells by unknown mechanisms. Here we address the question of how the silenced mRNA can be translationally activated. We show that hnRNP K and the c-Src kinase specifically interact with each other, leading to c-Src activation and tyrosine phosphorylation of hnRNP K in vivo and in vitro. c-Src-mediated phosphorylation reversibly inhibits the binding of hnRNP K to the differentiation control element (DICE) of the LOX mRNA 3′ untranslated region in vitro and specifically derepresses the translation of DICE-bearing mRNAs in vivo. Our results establish a novel role of c-Src kinase in translational gene regulation and reveal a mechanism by which silenced mRNAs can be translationally activated.

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Zekri, Latifa, Eric Huntzinger, Susanne Heimstädt, and Elisa Izaurralde. "The Silencing Domain of GW182 Interacts with PABPC1 To Promote Translational Repression and Degradation of MicroRNA Targets and Is Required for Target Release." Molecular and Cellular Biology 29, no. 23 (September 21, 2009): 6220–31. http://dx.doi.org/10.1128/mcb.01081-09.

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ABSTRACT GW182 family proteins are essential in animal cells for microRNA (miRNA)-mediated gene silencing, yet the molecular mechanism that allows GW182 to promote translational repression and mRNA decay remains largely unknown. Previous studies showed that while the GW182 N-terminal domain interacts with Argonaute proteins, translational repression and degradation of miRNA targets are promoted by a bipartite silencing domain comprising the GW182 middle and C-terminal regions. Here we show that the GW182 C-terminal region is required for GW182 to release silenced mRNPs; moreover, GW182 dissociates from miRNA targets at a step of silencing downstream of deadenylation, indicating that GW182 is required to initiate but not to maintain silencing. In addition, we show that the GW182 bipartite silencing domain competes with eukaryotic initiation factor 4G for binding to PABPC1. The GW182-PABPC1 interaction is also required for miRNA target degradation; accordingly, we observed that PABPC1 associates with components of the CCR4-NOT deadenylase complex. Finally, we show that PABPC1 overexpression suppresses the silencing of miRNA targets. We propose a model in which the GW182 silencing domain promotes translational repression, at least in part, by interfering with mRNA circularization and also recruits the deadenylase complex through the interaction with PABPC1.

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Dissertations / Theses on the topic "Translational silencing"

1

Kapasi, Purvi. "An Insight into GAIT Complex Mediated Translational Silencing." Cleveland State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=csu1232567504.

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Danner, Johannes [Verfasser], and Gunter [Akademischer Betreuer] Meister. "Regulation of gene silencing: From microRNA biogenesis to post-translational modifications of TNRC6 complexes / Johannes Danner ; Betreuer: Gunter Meister." Regensburg : Universitätsbibliothek Regensburg, 2017. http://d-nb.info/1172970572/34.

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Chiang, Jen-Chieh. "Dosage Compensation of Trisomy 21 and Its Implications for Hematopoietic Pathogenesis in Down Syndrome." eScholarship@UMMS, 2011. http://escholarship.umassmed.edu/gsbs_diss/931.

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Down Syndrome (DS), the most common aneuploidy seen in live-borns, is caused by trisomy for chromosome 21. DS imposes high risks for multiple health issues involving various systems of the body. The genetic complexity of trisomy 21 and natural variation between all individuals has impeded understanding of the specific cell pathologies and pathways involved. In addition, chromosomal disorders have been considered outside the hopeful progress in gene therapies for single-gene disorders. Here we test the feasibility of correcting imbalanced expression of genes across an extra chromosome by expression of a single gene, XIST, the key player in X chromosome inactivation. We targeted a large XIST transgene into one chromosome 21 in DS iPS cells, and demonstrated XIST RNA spreads and induces heterochromatin and gene silencing across that autosome in cis. By making XIST inducible, this allows direct comparison of effects of trisomy 21 expression on cell function and phenotypes. Importantly, XIST-induction during in vitro hematopoiesis normalized excess production of differentiated blood cell types (megakaryocytes and erythrocytes), known to confer high risk for myeloproliferative disorder and leukemia. In contrast, trisomy silencing enhances production of iPS and neural stem cells, consistent with DS clinical features. Further analysis revealed that trisomy 21 initially impacts the endothelial hematopoietic transition (EHT) to generate excess CD43+ progenitors, and also increases their colony forming potential. Furthermore, results provide evidence for a key role for enhanced IGF signaling, involving over-expression of non-chromosome 21 genes controlled by trisomy 21. Finally, experiments to examine trisomy effects on angiogenesis showed no effect on production of endothelial cells, but it remains unclear whether trisomic cells may differ in ability to form vessels. Collectively, this thesis demonstrates proof-of-principle for XIST-mediated “trisomy silencing”. Phenotypic improvement of hematopoietic and neural stem cells demonstrates the value for research into DS pathogenesis, but also provides a foundation of potential for future development of “chromosome therapy” for DS patients.

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4

Chiang, Jen-Chieh. "Dosage Compensation of Trisomy 21 and Its Implications for Hematopoietic Pathogenesis in Down Syndrome." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/931.

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Down Syndrome (DS), the most common aneuploidy seen in live-borns, is caused by trisomy for chromosome 21. DS imposes high risks for multiple health issues involving various systems of the body. The genetic complexity of trisomy 21 and natural variation between all individuals has impeded understanding of the specific cell pathologies and pathways involved. In addition, chromosomal disorders have been considered outside the hopeful progress in gene therapies for single-gene disorders. Here we test the feasibility of correcting imbalanced expression of genes across an extra chromosome by expression of a single gene, XIST, the key player in X chromosome inactivation. We targeted a large XIST transgene into one chromosome 21 in DS iPS cells, and demonstrated XIST RNA spreads and induces heterochromatin and gene silencing across that autosome in cis. By making XIST inducible, this allows direct comparison of effects of trisomy 21 expression on cell function and phenotypes. Importantly, XIST-induction during in vitro hematopoiesis normalized excess production of differentiated blood cell types (megakaryocytes and erythrocytes), known to confer high risk for myeloproliferative disorder and leukemia. In contrast, trisomy silencing enhances production of iPS and neural stem cells, consistent with DS clinical features. Further analysis revealed that trisomy 21 initially impacts the endothelial hematopoietic transition (EHT) to generate excess CD43+ progenitors, and also increases their colony forming potential. Furthermore, results provide evidence for a key role for enhanced IGF signaling, involving over-expression of non-chromosome 21 genes controlled by trisomy 21. Finally, experiments to examine trisomy effects on angiogenesis showed no effect on production of endothelial cells, but it remains unclear whether trisomic cells may differ in ability to form vessels. Collectively, this thesis demonstrates proof-of-principle for XIST-mediated “trisomy silencing”. Phenotypic improvement of hematopoietic and neural stem cells demonstrates the value for research into DS pathogenesis, but also provides a foundation of potential for future development of “chromosome therapy” for DS patients.

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5

Floris, Maïna. "Etude des régulations post-transcriptionnelles en réponse à la lumière chez Arabidopsis thaliana." Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM4005.

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Ce travail de thèse porte sur l’étude des régulations post-transcriptionnelles en réponse à la lumière chez A.thaliana. Nous avons étudié deux systèmes de réponse à la lumière, la régulation traductionnelle des antennes photosynthétiques (Lhc) et la régulation de la voie des anthocyanes par le RNA silencing permettant la photoprotection. Dans une première partie nôtre approche a permis de montrer que la lumière a un impact sur le niveau de traduction global. De plus nous avons pu mettre en évidence que certaines Lhc sont régulées de façon traductionnelles en réponse à la lumière. Cette régulation pourrait être une composante du signal rétrograde entre le chlorolaste et le noyau. En parrallèle dans une seconde partie nous avons caractérisé la voie TAS4 de RNA silencing chez les plantes. Cette voie est mise en place en réponse à la forte lumière et régule l’accumulation des anthocyanes
This work concerned post-transcriptional regulations in response to light in Arabidopsis thaliana. We are interested in two light responsive systems, translational regulation of the photosynthetic antenna protein and the regulation of the anthocyanin pathway by RNA silencing.In a first part we have shown that light affects global translation level. Furthermore our data indicate that some Lhc proteins are regulated at translational level in response to light. It seems that transaltional regulation of Lhc is a part of retrograde signaling between chlroroplast and nuclear. In a second part we have characterized the TAS4 RNA silencing pathway in Arabidopsis. We show that TAS4 regulate the accumulation of anthocyanin pathway in respose to high light

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6

Guidi, Mònica. "Micro RNA-Mediated regulation of the full-length and truncated isoforms of human neurotrophic tyrosine kinase receptor type 3 (NTRK 3)." Doctoral thesis, Universitat Pompeu Fabra, 2009. http://hdl.handle.net/10803/7114.

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Neurotrophins and their receptors are key molecules in the development of the
nervous system. Neurotrophin-3 binds preferentially to its high-affinity receptor
NTRK3, which exists in two major isoforms in humans, the full-length kinaseactive
form (150 kDa) and a truncated non-catalytic form (50 kDa). The two
variants show different 3'UTR regions, indicating that they might be differentially
regulated at the post-transcriptional level. In this work we explore how
microRNAs take part in the regulation of full-length and truncated NTRK3,
demonstrating that the two isoforms are targeted by different sets of microRNAs.
We analyze the physiological consequences of the overexpression of some of the
regulating microRNAs in human neuroblastoma cells. Finally, we provide
preliminary evidence for a possible involvement of miR-124 - a microRNA with no
putative target site in either NTRK3 isoform - in the control of the alternative
spicing of NTRK3 through the downregulation of the splicing repressor PTBP1.
Las neurotrofinas y sus receptores constituyen una familia de factores cruciales
para el desarrollo del sistema nervioso. La neurotrofina 3 ejerce su función
principalmente a través de una unión de gran afinidad al receptor NTRK3, del cual
se conocen dos isoformas principales, una larga de 150KDa con actividad de tipo
tirosina kinasa y una truncada de 50KDa sin dicha actividad. Estas dos isoformas
no comparten la misma región 3'UTR, lo que sugiere la existencia de una
regulación postranscripcional diferente. En el presente trabajo se ha explorado
como los microRNAs intervienen en la regulación de NTRK3, demostrando que las
dos isoformas son reguladas por diferentes miRNAs. Se han analizado las
consecuencias fisiológicas de la sobrexpresión de dichos microRNAs utilizando
células de neuroblastoma. Finalmente, se ha estudiado la posible implicación del
microRNA miR-124 en el control del splicing alternativo de NTRK3 a través de la
regulación de represor de splicing PTBP1.

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7

Lettrich, Patrik. "Translační iniciační faktory proteinové rodiny 4E a jejich vliv na regulaci genové exprese." Master's thesis, 2021. http://www.nusl.cz/ntk/nusl-446448.

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The translation represents one of the most crucial processes in the cell. That is why it is often targeted by various regulations. Its initiation phase has a particularly important role in regulatory processes. Initiation of translation usually starts by recognition and binding of canonical eukaryotic initiation factor 4E1 (eIF4E1) to the methylguanosine cap present on the 5' end of the majority of eukaryotic mRNA. The family of 4E translation initiation factors contains two more members - eIF4E2 and eIF4E3. Those two proteins can bind cap structure as well which predetermines it to function in the regulation of translation. Protein eIF4E2 is well known for being a translational repressor in development processes and it takes part in specific miRNA-dependent silencing. It was proven to be able to initiate translation in hypoxia which is consistent with its proposed role in hypoxic tumor cells. The biological roles of the protein eIF4E3 are much less understood. This thesis propounds the picture of the overall functions of all discussed translation initiation factors using cell lines with their overexpression or deletion. Experimental data confirmed the role of the eIF4E2 in the regulation of developmental processes. Cell lines with deleted eIF4E2 and eIF4E3 were characterized based on the influence...

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Books on the topic "Translational silencing"

1

S, Cho-Chung Yoon, Gewirtz A. M, Stein Cy A, and New York Academy of Sciences., eds. Therapeutic oligonucleotides: Transcriptional and translational strategies for silencing gene expression. New York: New York Academy of Sciences, 2005.

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2

Rhoads, Robert E. MiRNA regulation of the translational machinery. Edited by SpringerLink (Online service). Berlin: Springer, 2009.

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3

Grande, Morales Julio, ed. Silencio. Madrid: Alianza Editorial, 2011.

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4

Letelier-Ruz, Elias. Silence =: Silencio. Dorion, Quebec: The Muses' Company, 1992.

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5

El honor del silencio. Barcelona: Plaza & Janes, 1997.

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6

1926-, Reid Alastair, and Heebner Mary, eds. On the blue shore of silence: Poems of the sea = A la orilla azul del silencio : poemas del mar. New York: Rayo, 2003.

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Cho-Chung, Yoon S., Cy A. Stein, Cooley's Anemia Symposium 2005 Lake Buen, Elliott P. Vichinsky, and NIH SYMPOSIUM ON THERAPEUTIC OLIGONUCLEO. Therapeutic Oligonucleotides: Transcriptional and translational Strategies for Silencing Gene Expression (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2006.

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Stein, Cy A., and A. M. Gewirtz. Therapeutic Oligonucleotides: Transcriptional and Translational Strategies for Silencing Gene Expression (Annals of the New York Academy of Sciences). Blackwell Publishing Limited, 2005.

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9

Simons, Margaret A. The Silencing of Simone de Beauvoir. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190608811.003.0004.

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This chapter, first published in 1983, initially breaks the news of the scandal of the first English translation of Le deuxième sexe to the English speaking world. Through a painstaking comparative reading of the Parshley translation, published by Knopf, alongside the original French, the chapter reveals the abridgment and editing of the original text with no indication of specific cuts in the text. It shows that Parshley’s version of The Second Sex exhibits a sexist pattern of selection that reduces the impact of Beauvoir’s discussions of women’s history; drastically reduces the number of references to women writers, poets, politicians, military figures, etc.; curtails discussions of women’s oppression; and obscures Beauvoir’s philosophical commitments. This text was the first of those that ignited the flood of contemporary Beauvoir scholarship in the English-speaking world. It was because of Margaret Simon’s work that Beauvoir became aware of the flawed translation shortly before her death in 1986, and expressed her ardent wish for a new translation.

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10

Ma'yuk sti'ilal xch'inch'unel k'inal: Silencio sin frontera : poemas y cuentos. San Cristóbal de las Casas, Chiapas: Secretaría de Pueblos y Culturas Indígenas, 2011.

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Book chapters on the topic "Translational silencing"

1

Paro, Renato, Ueli Grossniklaus, Raffaella Santoro, and Anton Wutz. "RNA-Based Mechanisms of Gene Silencing." In Introduction to Epigenetics, 117–33. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68670-3_6.

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AbstractAlthough epigenetic states are typically associated with DNA-methylation and posttranslational histone modifications, RNAs often play an important role in their regulation. Specific examples have already been discussed in the context of dosage compensation (see book ► Chap. 10.1007/978-3-030-68670-3_4 of Wutz) and genomic imprinting (see book ► Chap. 10.1007/978-3-030-68670-3_5 of Grossniklaus). In this Chapter, we will take a closer look at a particular class of RNAs implicated in gene silencing. Although the focus will lie on RNA-based silencing mechanisms in plants, many of its components, such as RNase III-related DICERLIKE endonucleases or small RNA-binding ARGONAUTE proteins, are conserved in animals, plants, and fungi. On the one hand, small RNAs are involved in post-transcriptional silencing by targeting mRNAs for degradation or inhibiting their translation, a feature that has been exploited for large-scale genetic screens. On the other hand, they also play a central role in transcriptional gene silencing, for instance in the repression of transposable elements across a wide variety of organisms. In plants, this involves a complex system whereby small RNAs derived from transposons and repeats direct DNA-methylation and repressive histone modifications in a sequence-specific manner. Recent results link this so-called RNA-dependent DNA-methylation to paramutation, a classical epigenetic phenomenon where one allele directs a heritable epigenetic change in another.

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Gargantini, Pablo R., César G. Prucca, and Hugo D. Luján. "Post-transcriptional Gene Silencing and Translation in Giardia." In Giardia, 233–44. Vienna: Springer Vienna, 2011. http://dx.doi.org/10.1007/978-3-7091-0198-8_15.

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Pantuchowicz, Agnieszka. "On Gender Silencing in Translation: A Case Study in Poland." In Language and Literature in a Glocal World, 127–36. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-8468-3_8.

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Pager, Cara T., Karen A. Wehner, Gabriele Fuchs, and Peter Sarnow. "Chapter 5 MicroRNA-Mediated Gene Silencing." In Progress in Molecular Biology and Translational Science, 187–210. Elsevier, 2009. http://dx.doi.org/10.1016/s1877-1173(09)90005-9.

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Wutz, Anton. "RNA-Mediated Silencing Mechanisms in Mammalian Cells." In Progress in Molecular Biology and Translational Science, 351–76. Elsevier, 2011. http://dx.doi.org/10.1016/b978-0-12-387685-0.00011-1.

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Cheunsuchon, Pornsuk, Yunli Zhou, Xun Zhang, Hang Lee, Wendy Chen, Yuki Nakayama, Kimberley A. Rice, E. Tessa Hedley-Whyte, Brooke Swearingen, and Anne Klibanski. "Silencing of the ImprintedDLK1-MEG3Locus in Human Clinically Non-Functioning Pituitary Adenomas." In BASIC/TRANSLATIONAL - Pituitary Biology & Tumorigenesis, P1–391—P1–391. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p2.p1-391.

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Song, Sang-houn, Kyong-ha So, Yutaka Suzuki, Yuya Kikuchi, Astrid Ardiyanti, Katsuyoshi Sato, Sang-gun Roh, and Kazuo Katoh. "Analysis of the Expression Profile in 3T3-L1 Adipocytes by shRNA-Mediated Silencing of Adipogenin Gene." In BASIC/TRANSLATIONAL - Endocrine Influence on Adipose Tissue, P2–426—P2–426. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part3.p2.p2-426.

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Blackmore, Julia Kristine, Vaishali Chaubal, Sudipan Karmakar, and Carolyn Louise Smith. "The Silencing Mediator of Retinoic Acid and Thyroid Hormone Receptor (SMRT) Coregulator Promotes Breast Carcinogenesis through Multiple Cellular Pathways." In BASIC/TRANSLATIONAL - Hormones & Breast Cancer, P1–59—P1–59. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part1.p3.p1-59.

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Chaiwangyen, Wittaya. "The Impact of Dietary Compounds in Functional Foods on MicroRNAs Expression." In Functional Foods [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96746.

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MicroRNAs (miRNAs) are a class of non-coding endogenous RNA molecules that are involved in post-transcriptional gene silencing via binding to their target messenger RNA, leading to mRNA degradation or translational repression. MicroRNAs can be modulated by several factors including hormones, transcription factors, and dietary compounds. These biologically active compounds have positive impact on the progression of human pathology including non-communicable diseases, which indicating that administration of diet may have potential as therapeutic agents in modulating the risk of chronic diseases. Interestingly, evidence emerging in recent years suggests that dietary miRNAs can be absorbed in human circulation, modulated human gene expression and biological functions. The exploitation of the miRNA functioning within different origins, cellular miRNAs and dietary miRNAs will help us to understand the molecular machinery as well as the regulatory mechanisms involved in fundamentally important biological processes. Therefore, this knowledge may be applied of natural bioactive compounds in preventive or therapeutic approaches.

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Tyulenev, Sergey. "Speaking Silence and Silencing Speech." In Queering Translation, Translating the Queer, 112–29. Routledge, 2017. http://dx.doi.org/10.4324/9781315505978-9.

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Conference papers on the topic "Translational silencing"

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Leibowitz-Amit, Raya, Liron Zehavi, Dror Avni, and Yehezkel Sidi. "Abstract A17: miRNA silencing in malignant melanoma: Mechanisms, regulation, and potential implications." In Abstracts: AACR International Conference on Translational Cancer Medicine--; Mar 21–24, 2010; Amsterdam, The Netherlands. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1078-0432.tcme10-a17.

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Samanta, R., J. Dunning, A. Taylor, EMINENT:ARDS Investigators, MOSAIC Investigators, E. R. Chilvers, R. C. Chambers, P. J. Openshaw, and C. Summers. "Severe Respiratory Failure in Adult Influenza Infection Is Characterised by Mechanisms Relating to Pulmonary Endothelial Leak and Interferon Gamma Induced Translational Silencing." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5288.

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