Gotowe bibliografie tematyczne / Post-transcriptional gene regulation

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  1. Artykuły w czasopismach
  2. Rozprawy doktorskie
  3. Książki
  4. Części książek
  5. Streszczenia konferencji
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Gotowa bibliografia na temat „Post-transcriptional gene regulation”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 21 lutego 2023

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Artykuły w czasopismach na temat "Post-transcriptional gene regulation"

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Tew, Simon R., i Peter D. Clegg. "Post-transcriptional gene regulation in chondrocytes". Biochemical Society Transactions 38, nr 6 (24.11.2010): 1627–31. http://dx.doi.org/10.1042/bst0381627.

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The control of gene expression in articular chondrocytes is an essential factor in maintaining the homoeostasis of extracellular matrix synthesis and turnover necessary in healthy articular cartilage. Although much is known of how steady-state levels of gene expression and rates of transcription are altered, there has been a poorer understanding of gene control at the post-transcriptional level and its relevance to cartilage health and disease. Now, an emerging picture is developing of the importance of this tier of gene regulation, driven by in vitro studies and mouse genetic models. This level of cellular regulation represents an as yet unexplored area of potential intervention for the treatment of degenerative cartilage disorders such as osteoarthritis.
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Lipshitz, Howard D., Julie M. Claycomb i Craig A. Smibert. "Post-transcriptional regulation of gene expression". Methods 126 (sierpień 2017): 1–2. http://dx.doi.org/10.1016/j.ymeth.2017.08.007.

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Kashanchi, Fatah, i John N. Brady. "Transcriptional and post-transcriptional gene regulation of HTLV-1". Oncogene 24, nr 39 (wrzesień 2005): 5938–51. http://dx.doi.org/10.1038/sj.onc.1208973.

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Alonso, C. R. "Post-transcriptional gene regulation via RNA control". Briefings in Functional Genomics 12, nr 1 (1.01.2013): 1–2. http://dx.doi.org/10.1093/bfgp/els060.

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Zhao, Boxuan Simen, Ian A. Roundtree i Chuan He. "Post-transcriptional gene regulation by mRNA modifications". Nature Reviews Molecular Cell Biology 18, nr 1 (3.11.2016): 31–42. http://dx.doi.org/10.1038/nrm.2016.132.

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Swaminathan, Sankar. "Post-transcriptional gene regulation by gamma herpesviruses". Journal of Cellular Biochemistry 95, nr 4 (2005): 698–711. http://dx.doi.org/10.1002/jcb.20465.

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Sadelain, Michel. "Transcriptional and post transcriptional gene regulation in stem cell-based gene therapy". Blood Cells, Molecules, and Diseases 40, nr 2 (marzec 2008): 283. http://dx.doi.org/10.1016/j.bcmd.2007.10.074.

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Kuhlemier, Cris. "Transcriptional and post-transcriptional regulation of gene expression in plants". Plant Molecular Biology 19, nr 1 (maj 1992): 1–14. http://dx.doi.org/10.1007/bf00015603.

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Ray, Swagat, Pól Ó. Catnaigh i Emma C. Anderson. "Post-transcriptional regulation of gene expression by Unr". Biochemical Society Transactions 43, nr 3 (1.06.2015): 323–27. http://dx.doi.org/10.1042/bst20140271.

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Unr (upstream of N-ras) is a eukaryotic RNA-binding protein that has a number of roles in the post-transcriptional regulation of gene expression. Originally identified as an activator of internal initiation of picornavirus translation, it has since been shown to act as an activator and inhibitor of cellular translation and as a positive and negative regulator of mRNA stability, regulating cellular processes such as mitosis and apoptosis. The different post-transcriptional functions of Unr depend on the identity of its mRNA and protein partners and can vary with cell type and changing cellular conditions. Recent high-throughput analyses of RNA–protein interactions indicate that Unr binds to a large subset of cellular mRNAs, suggesting that Unr may play a wider role in translational responses to cellular signals than previously thought.
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Sánchez-Jiménez, Flora, i Víctor Sánchez-Margalet. "Role of Sam68 in Post-Transcriptional Gene Regulation". International Journal of Molecular Sciences 14, nr 12 (28.11.2013): 23402–19. http://dx.doi.org/10.3390/ijms141223402.

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Rozprawy doktorskie na temat "Post-transcriptional gene regulation"

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Hayden, Celine. "Post-Transcriptional Gene Regulation in Plants". Diss., Tucson, Arizona : University of Arizona, 2006. http://etd.library.arizona.edu/etd/GetFileServlet?file=file:///data1/pdf/etd/azu%5Fetd%5F1684%5F1%5Fm.pdf&type=application/pdf.

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Martins, Rute Isabel Paulo. "Post-transcriptional regulation of HFE gene expression". Doctoral thesis, FCT - UNL, 2010. http://hdl.handle.net/10362/5596.

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Thesis presented to obtain the Ph.D. degree in Biology (Molecular Genetics), by the Universidade Nova de Lisboa, Faculdade de Ciências e Tecnologia.
O ferro é um elemento essencial em diversos processos metabólicos celulares. O desafio que se coloca para a maioria dos organismos prende-se com o controlo do ferro absorvido de modo a suprir as necessidades destes processos evitando, no entanto, os danos causados pelo ferro livre. Na realidade, algumas das doenças humanas mais comuns estão relacionadas com a perturbação da homeostase do ferro. Entre estas, encontra-se a hemocromatose hereditária que, estando maioritariamente associada a mutações no gene HFE, origina a acumulação de ferro em vários órgãos. A proteína HFE actua na homeostase do ferro através da regulação da expressão da hepcidina no fígado. O principal transcrito HFE apresenta baixos níveis de expressão numa série de tecidos humanos, tendo sido descritos diversos transcritos adicionais. O trabalho aqui apresentado aborda a caracterização dos transcritos alternativos de HFE, os mecanismos envolvidos na sua génese, assim como o seu possível papel fisiológico e regulação. A análise de diversos tecidos humanos permitiu identificar vários transcritos HFE resultantes de splicing alternativo. O estudo funcional de algumas proteínas correspondentes demonstrou que o processo de splicing alternativo pode gerar variantes não funcionais ou produzir uma variante HFE solúvel que é secretada pelas células associada à beta2-microglobulina. Esta proteína poderá desempenhar um papel crucial na homeostase do ferro, actuando como um agonista ou antagonista da HFE full length. Além disso, foi demonstrado que a expressão do transcrito HFE principal é fisiologicamente regulada pelo mecanismo de nonsense-mediated mRNA decay (NMD), dado que os seus níveis aumentam quando este mecanismo é inibido. A pesquisa realizada em tecidos humanos permitiu verificar que a expressão do mRNA HFE resulta da utilização de quatro locais de clivagem e poliadenilação alternativos. Este padrão de poliadenilação alternativa específico de tecido aparenta responder a estímulos de ferro, actuando coordenadamente com o NMD no ajustamento dos níveis de expressão de HFE. Esta dissertação demonstra que a regulação da expressão do gene HFE é influenciada pós-transcricionalmente pelos mecanismos de splicing alternativo, poliadenilação alternativa e NMD. Este conhecimento poderá conduzir a novas perspectivas de investigação na área do metabolismo do ferro e contribuir para o delinear de novas estratégias terapêuticas a aplicar em patologias de homeostase do ferro através da regulação da hepcidina.
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Mavropoulos, Athanasios. "Post-transcriptional regulation of interferon-γ gene expression". Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415673.

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Jones, Christopher Iain. "Post-transcriptional gene regulation by the exoribonuclease pacman". Thesis, University of Brighton, 2011. https://research.brighton.ac.uk/en/studentTheses/ff276681-fead-45e4-842f-df0c3a44cfce.

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The gene pacman (pcm) in Drosophila melanogaster encodes the exoribonuclease XRN1, which is highly conserved across eukaryotes and is the only known cytoplasmic exoribonuclease that degrades RNA in the 5’ – 3’ direction. Hypomorphic mutations to pacman have previously been shown cause developmental phenotypes, particularly during wing and thorax development. The focus of this thesis was twofold. Firstly, to create a null pacman allele and associated control lines to further characterise the phenotypes of pcm. Two new alleles were created, one of which was amorphic (pcm14). pcm14 is 100% lethal, and flies die during pupation. The wing imaginal discs of pcm14 larvae are less than half the size of those in wild‐type larvae at the same stage (3rd instar). It was also found that wing imaginal discs in the hypomorphic mutant pcm5 are significantly smaller than wild‐type, by almost 20%. Therefore, pcm appears to play a role in cell proliferation or apoptosis during the growth of wing imaginal discs. Along with pcm14, a new deficiency that includes pcm was created using a DrosDel Rearrangement Screen. The 17,963bp Df(1)ED7452 deficiency is >13 times smaller than the two other publically available deficiencies that include pcm.
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Begbie, Megan Elaine. "Transcriptional and post-transcriptional regulation of the human factor VIII gene". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0021/NQ45262.pdf.

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Liu, Jun-Li. "Transcriptional and post-transcriptional regulation of somatostatin gene expression by glucocorticoids". Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=28826.

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Glucocorticoids and somatostatin both influence a broad spectrum of biological activities and their actions are cooperative in growth control, pancreatic islet function, immune suppression, and stress response, e.g. in vivo studies indicate that glucocorticoids may act through somatostatin to suppress growth, growth hormone secretion and inflammation. Recent studies have suggested that glucocorticoids influence somatostatin production but the precise nature of this effect has remained unclear. In this thesis, I characterized the actions of glucocorticoids on somatostatin gene expression and their molecular mechanisms of action in three consecutive studies. (1) I started with an investigation of the in vivo and in vitro effects of glucocorticoids and found that dexamethasone exerts significant effects on somatostatin peptide and steady state mRNA levels in normal somatostatinoma (1027B$ sb2$) cells. Glucocorticoids stimulate somatostatin production in peripheral tissues (stomach, pancreas, and jejunum) and suppress its biosynthesis in cerebral cortex and hypothalamus. Glucocorticoids induce dose-dependent biphasic effects on steady state somatostatin-mRNA levels in normal rat islet and 1027B$ sb2$ cells, characterized by stimulation at low doses (10$ sp{-10}$ M) and marked inhibition at high doses ($ geq$10$ sp{-7}$ M). This suggests a complex molecular mechanisms of glucocorticoid action on the somatostatin gene involving multi-level regulation. (2) I further discovered that glucocorticoids stimulate somatostatin gene transcription in PC12 (pheochromocytoma) cells transfected with somatostatin promoter-CAT (chloramphenicol acetyl transferase) reporter gene. Dexamethasone induces a dose-dependent 2.2 fold stimulation of somatostatin-CAT expression in PC12 cells and exerts an additive effect on cAMP-induced gene transcription. The dexamethasone effect is abolished in A126-1B2 (protein kinase A-deficient mutant PC12) cells and with CRE (cAMP response element) mutant
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Brown, Naomi Jane. "Post-transcriptional regulation of the pea plastocyanin gene (PetE)". Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597002.

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Expression of the pea plastocyanin gene (PetE) is regulated both by light and by signals from the chloroplast. Previous work has indicated that the light and chloroplast-controlled regulation operates post-transcriptionally in transgenic tobacco, requiring the correct 5’ terminus of the transcript and elements within the plastocyanin-coding region. The post-transcriptional light and chloroplast-controlled regulation of pea PetE has now been demonstrated to operate in transgenic Arabidopsis plants, indicating that the regulation is conserved in an additional plant species. The overall aim of the research described in this dissertation was to investigate the mechanisms by which light and plastid signals influence the stability of PetE transcripts. PetE constructs containing premature stop codons in the coding region were generated to investigate whether translation has a role in the light or chloroplast-controlled regulation. RNA-gel-blot analysis of transgenic plants containing these constructs was used to examine the effects of light and plastid inhibitors on pea PetE transcript accumulation in 7-day-old tobacco seedlings. The results obtained suggested that translation of the start of the PetE coding region is required for both light and plastid-regulated transcript stability. Constructs containing progressive 3’ deletions of the PetE coding region, fused to the Luc reporter gene, were generated to examine how much of the coding sequence is necessary for the regulation. Luciferase assays and RNA-gel-blot analysis were carried out on transgenic tobacco seedlings containing the constructs, to examine the effects of light and plastid inhibitors on the regulation. The results indicated that an element important in the light and chloroplast-controlled regulation is located in the first 12% of the coding region, corresponding to the first 60 nucleotides. The start of the plastocyanin-coding region therefore appears to contain sequences important in the regulation by light and plastid signals, and these sequences may need to be translated in order for the regulation to operate.
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Jia, Tao. "Stochastic Modeling of Gene Expression and Post-transcriptional Regulation". Diss., Virginia Tech, 2011. http://hdl.handle.net/10919/28483.

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Stochasticity is a ubiquitous feature of cellular processes such as gene expression that can give rise to phenotypic differences for genetically identical cells. Understanding how the underlying biochemical reactions give rise to variations in mRNA/protein levels is thus of fundamental importance to diverse cellular processes. Recent technological developments have enabled single-cell measurements of cellular macromolecules which can shed new light on processes underlying gene expression. Correspondingly, there is a need for the development of theoretical tools to quantitatively model stochastic gene expression and its consequences for cellular processes. In this dissertation, we address this need by developing general stochastic models of gene expression. By mapping the system to models analyzed in queueing theory, we derive analytical expressions for the noise in steady-state protein distributions. Furthermore, given that the underlying processes are intrinsically stochastic, cellular regulation must be designed to control the`noise' in order to adapt and respond to changing environments. Another focus of this dissertation is to develop and analyze stochastic models of post-transcription regulation. The analytical solutions of the models proposed provide insight into the effects of different mechanisms of regulation and the role of small RNAs in fine-tunning the noise in gene expression. The results derived can serve as building blocks for future studies focusing on regulation of stochastic gene expression.
Ph. D.
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Rozanska, Agata. "Regulation of post-transcriptional gene expression in human mitochondria". Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2706.

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Mitochondria are cellular organelles that have evolved from the eubacterial ancestor into highly specialized compartment of the eukaryotic cell. They are unique among animal cells in that they retain a level of autonomy through the genetic information in their genome. Human mtDNA is built of ~16.5 kbp encoding 13 polypeptides, which are synthesised by mitoribosomes. The latter consist of two RNA species also transcribed from mtDNA and approximately 80 proteins originating from the nucleus. All 13 products of intramitochondrial translation are incorporated into the inner mitochondrial membrane where they co-build the oxidative phosphorylation (OXPHOS) system. OXPHOS is a multicomplex machinery, the final product of which is adenosine triphosphate, ATP, a carrier of energy that is necessary to sustain cell homeostasis and growth. The malfunctions of mitochondria have a severe impact on the ‘host’ organism and are the causative factor in many human diseases. Pathological changes of mitochondrial function can be triggered by mutations in the mitochondrial genome and/or defects in nuclear genes involved in mitochondrial activity. The mitochondrial gene expression pathway has been increasingly investigated during last twenty years and combines both types of factors, those translated in the cytosol and those synthesised in the mitochondrial matrix. A functional mitochondrion requires over 1500 proteins to be imported from the cytosol, a significant subset of these are devoted to the maintenance, replication, transcription and subsequently for translation of the minimal mitochondrial genome fostered within. In the course of my PhD study three of these nuclear encoded but mitochondrially destined proteins were investigated. The first of these proteins that I contributed to investigating was SLIRP. As the specificity of this RNA binding protein had not been established I performed CLIP (cross-linking immunoprecipitation) assay in order to assess the ability of SLIRP to bind RNA. The data generated from this analysis directly showed that SLIRP can interact with all mt-mRNAs apart from MTND6. This work confirmed that SLIRP participates in the stability of mt-mRNA species, as has now been subsequently published by other research groups. A main part of my PhD studies centred on characterisation of MRPL12. This protein belongs to the pool of conserved mitochondrial proteins having the bacterial orthologue 3 called L7/L12. One of the unique features of these proteins is their dynamic character and ability to exchange location between ribosomal LSU and the free pool. This has been postulated to be a regulatory mechanism of translation process in response to fluctuations in cell metabolism. To test this hypothesis I characterised immortalised fibroblasts obtained from a patient with a homozygous mutation in MRPL12 caused by c.542C to T transition in exon 5. This cell line allowed me to study the consequence of this defect on the regulation of translation in human mitochondria. I could conclude that a reduced number of MRPL12 molecules per mt-LSU in subject fibroblasts did not affect overall mitoribosome assembly, but a visible decline in mitochondrial translation was detected although the reduction in translational efficiency for different mitochondrially encoded subunits varied. The third protein that I characterised was mitochondrial RBFA. This protein was identified in my host laboratory and preliminary characterisation performed prior to my involvement. My studies included the CLIP assay that showed direct interaction of this protein with a 3’ terminal stem loop of helix 45 of the 12S mt-rRNA. The methylation status of two conserved neighbouring adenines located in helix 45 was altered by changes in steady state level of RBFA. Moreover, the CLIP data identified a second rRNA species associated with RBFA. This was an unexpected RNA species in the form of 5S rRNA. The data regarding the mitochondrial localisation and specifically any submitochondrial location has been controversial. Intriguingly my data identified a number of chimeric CLIP sequences containing both 5S and 12S rRNA fragments, strongly suggesting that within the mitochondrial matrix RBFA interacts simultaneously with both RNA species. Similarity between the 5S rRNA secondary structure and snoRNA, which guides modifications on cytosolic rRNA, led to the hypothesis proposing a novel function for 5S rRNA guiding methylation at helix 45 of the 12S mtrRNA. My data therefore assign RBFA as a new member of the group of maturation factors of the mammalian mt-SSU.
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Elgamal, Ola A. "TRANSCRIPTIONAL AND POST TRANSCRIPTIONAL REGULATION OF GENE EXPRESSION: APPLICATIONS TO BIOLOGY AND CANCER". The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1461071345.

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Książki na temat "Post-transcriptional gene regulation"

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Dassi, Erik, red. Post-Transcriptional Gene Regulation. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1851-6.

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Wilusz, Jeffrey, red. Post-Transcriptional Gene Regulation. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-033-1.

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Dassi, Erik, red. Post-Transcriptional Gene Regulation. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3067-8.

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NATO/CEC, Advanced Research Workshop on "Post-Transcriptional Control of Gene Expression" (1990 Goslar Germany). Post-transcriptional control of gene expression. Berlin: Springer-Verlag, 1990.

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Wajapeyee, Narendra, i Romi Gupta, red. Eukaryotic Transcriptional and Post-Transcriptional Gene Expression Regulation. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6518-2.

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B, Harford Joe, i Morris David R. 1939-, red. mRNA metabolism & post-transcriptional gene regulation. New York: Wiley-Liss, 1997.

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Maxim, Golovkin, i SpringerLink (Online service), red. Nuclear pre-mRNA Processing in Plants. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2008.

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Henri, Grosjean, red. Fine-tuning of RNA functions by modification and editing. Berlin: Springer, 2005.

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Jeffrey, Wilusz, red. Post-transcriptional gene regulation. Totowa, N.J: Humana Press, 2008.

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Dassi, Erik. Post-Transcriptional Gene Regulation. Springer New York, 2016.

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Części książek na temat "Post-transcriptional gene regulation"

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Bagga, Paramjeet S. "Bioinformatics Approaches for Studying Untranslated Regions of mRNAs". W Post-Transcriptional Gene Regulation, 1–21. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-033-1_1.

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Bajak, Edyta Z., i Curt H. Hagedorn. "Efficient 5' Cap-Dependent RNA Purification: Use in Identifying and Studying Subsets of RNA". W Post-Transcriptional Gene Regulation, 147–60. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-033-1_10.

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Venables, Julian P. "Enrichment of Alternatively Spliced Isoforms". W Post-Transcriptional Gene Regulation, 161–70. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-033-1_11.

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Hague, Lisa K., Tyra Hall-Pogar i Carol S. Lutz. "In Vivo Methods to Assess Polyadenylation Efficiency". W Post-Transcriptional Gene Regulation, 171–85. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-033-1_12.

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Long, Roy M., i Carl R. Urbinati. "Monitoring the Temporal and Spatial Distribution of RNA in Living Yeast Cells". W Post-Transcriptional Gene Regulation, 187–96. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-033-1_13.

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Stephens, Samuel B., Rebecca D. Dodd, Rachel S. Lerner, Brook M. Pyhtila i Christopher V. Nicchitta. "Analysis of mRNA Partitioning Between the Cytosol and Endoplasmic Reticulum Compartments of Mammalian Cells". W Post-Transcriptional Gene Regulation, 197–214. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-033-1_14.

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Peng, Jing, Elizabeth L. Murray i Daniel R. Schoenberg. "In Vivo and In Vitro Analysis of Poly(A) Length Effects on mRNA Translation". W Post-Transcriptional Gene Regulation, 215–30. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-033-1_15.

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Eldad, Naama, i Yoav Arava. "A Ribosomal Density-Mapping Procedure to Explore Ribosome Positions Along Translating mRNAs". W Post-Transcriptional Gene Regulation, 231–42. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-033-1_16.

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Olivas, Wendy M. "Identification of Changes in Gene Expression by Quantitation of mRNA Levels". W Post-Transcriptional Gene Regulation, 243–58. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-033-1_17.

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Murray, Elizabeth L., i Daniel R. Schoenberg. "Application of the Invader® RNA Assay to the Polarity of Vertebrate mRNA Decay". W Post-Transcriptional Gene Regulation, 259–76. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-033-1_18.

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Streszczenia konferencji na temat "Post-transcriptional gene regulation"

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Pinard, Desre. "Eucalyptus grandis organellar gene transcriptional and post-transcriptional regulation in developing xylem". W ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1053020.

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Ogul, Hasan, i Giray S. Ozcan. "A framework for integrative analysis of transcriptional and post-transcriptional gene regulation". W 2013 7th International Conference on Application of Information and Communication Technologies (AICT). IEEE, 2013. http://dx.doi.org/10.1109/icaict.2013.6722723.

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BLENCOWE, BENJAMIN, STEVEN BRENNER, TIMOTHY HUGHES i QUAID MORRIS. "POST-TRANSCRIPTIONAL GENE REGULATION: RNA-PROTEIN INTERACTIONS, RNA PROCESSING, MRNA STABILITY AND LOCALIZATION". W Proceedings of the Pacific Symposium. WORLD SCIENTIFIC, 2008. http://dx.doi.org/10.1142/9789812836939_0052.

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Carrere-Molina, Jordi, Laia Subirats i Jordi Casas-Roma. "Towards an Analysis of Post-Transcriptional Gene Regulation in Psoriasis via microRNAs using Machine Learning Algorithms". W 2019 IEEE 32nd International Symposium on Computer-Based Medical Systems (CBMS). IEEE, 2019. http://dx.doi.org/10.1109/cbms.2019.00125.

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Olkhov-Mitsel, Ekaterina, Theodorus Van der Kwast, Ken Kron, Hilmi Ozcelik, Laurent Briollais, Neil Fleshner, Eleftherios Diamandis, Alexandre Zlotta i Bharati Bapat. "Abstract B21: Epigenetic and post-transcriptional regulation of the kallikrein gene family as a novel panel of prostate cancer biomarkers". W Abstracts: AACR Special Conference on Chromatin and Epigenetics in Cancer - June 19-22, 2013; Atlanta, GA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.cec13-b21.

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Mazan-Mamczarz, Krystyna, Patrick Hagner, Bojie Dai, Zhenqiu Liu i Ronald B. Gartenhaus. "Abstract 1249: The role of ATM-dependent Chk2 activation on post-transcriptional gene regulation by RNA-binding protein, HuR: implications for lymphoma development in AT patients". W Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1249.

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Tanwer, Pooja, i Daman Saluja. "P623 Post-transcriptional regulation of genes by non-coding RNA inneisseria gonorrhoeae, an obligate human pathogen". W Abstracts for the STI & HIV World Congress (Joint Meeting of the 23rd ISSTDR and 20th IUSTI), July 14–17, 2019, Vancouver, Canada. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/sextrans-2019-sti.691.

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Raporty organizacyjne na temat "Post-transcriptional gene regulation"

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Long-Sheng, Chang. Post Transcriptional Regulation of the Neurofibromatosis 2 Gene. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2004. http://dx.doi.org/10.21236/ada428293.

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Chang, Long-Sheng. Post Transcriptional Regulation of the Neurofibromatosis 2 Gene. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2003. http://dx.doi.org/10.21236/ada420890.

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Kuchka, M. R. Post transcriptional regulation of chloroplast gene expression by nuclear encoded gene products. Office of Scientific and Technical Information (OSTI), styczeń 1992. http://dx.doi.org/10.2172/7309627.

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Kuchka, M. R. Post transcriptional regulation of chloroplast gene expression by nuclear encoded gene products. Office of Scientific and Technical Information (OSTI), styczeń 1992. http://dx.doi.org/10.2172/5268747.

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Kuchka, M. R. Post-transcriptional regulation of chloroplast gene expression by nuclear encoded gene products. Office of Scientific and Technical Information (OSTI), sierpień 1999. http://dx.doi.org/10.2172/764181.

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Karen S. Browning, Marie Petrocek i Bonnie Bartel. The 5th Symposium on Post-Transcriptional Regulation of Plant Gene Expression (PTRoPGE). Office of Scientific and Technical Information (OSTI), czerwiec 2006. http://dx.doi.org/10.2172/889783.

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Kuchka, M. R. Post transcriptional regulation of chloroplast gene expression by nuclear encoded gene products. Progress report, June 1, 1991--May 31, 1992. Office of Scientific and Technical Information (OSTI), maj 1992. http://dx.doi.org/10.2172/10142165.

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Kuchka, M. R. Post transcriptional regulation of chloroplast gene expression by nuclear encoded gene products. Progress report, June 1, 1990--June 30, 1992. Office of Scientific and Technical Information (OSTI), sierpień 1992. http://dx.doi.org/10.2172/10161582.

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Whitham, Steven A., Amit Gal-On i Victor Gaba. Post-transcriptional Regulation of Host Genes Involved with Symptom Expression in Potyviral Infections. United States Department of Agriculture, czerwiec 2012. http://dx.doi.org/10.32747/2012.7593391.bard.

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Understanding how RNA viruses cause disease symptoms in their hosts is expected to provide information that can be exploited to enhance modern agriculture. The helper component-proteinase (HC-Pro) protein of potyviruses has been implicated in symptom development. Previously, we demonstrated that symptom expression is associated with binding of duplex small-interfering-RNA (duplex-siRNA) to a highly conserved FRNK amino acid motif in the HC-Pro of Zucchini yellow mosaic virus (ZYMV). This binding activity also alters host microRNA (miRNA) profiles. In Turnip mosaic virus (TuMV), which infects the model plant Arabidopsis, mutation of the FRNK motif to FINK was lethal providing further indication of the importance of this motif to HC-Pro function. In this continuation project, our goal was to further investigate how ZYMV and TuMV cause the mis-expression of genes in cucurbits and Arabidopsis, respectively, and to correlate altered gene expression with disease symptoms. Objective 1 was to examine the roles of aromatic and positively charged residues F164RNH and K215RLF adjacent to FR180NK in small RNA binding. Objective 2 was to determine the target genes of the miRNAs which change during HC-Pro expression in infected tissues and transgenic cucumber. Objective 3 was to characterize RNA silencing mechanisms underlying differential expression of host genes. Objective 4 was to analyze the function of miRNA target genes and differentially expressed genes in potyvirus-infected tissues. We found that the charged K/R amino acid residues in the FKNH and KRLF motifs are essential for virus viability. Replacement of K to I in FKNH disrupted duplex-siRNA binding and virus infectivity, while in KRLF mutants duplex-siRNA binding was maintained and virus infectivity was limited: symptomless following a recovery phenomenon. These findings expanded the duplex-siRNA binding activity of HC-Pro to include the adjacent FRNK and FRNH sites. ZYMV causes many squash miRNAs to hyper-accumulate such as miR166, miR390, mir168, and many others. Screening of mir target genes showed that only INCURVATA-4 and PHAVOLUTA were significantly upregulated following ZYMVFRNK infection. Supporting this finding, we found similar developmental symptoms in transgenic Arabidopsis overexpressing P1-HC-Pro of a range of potyviruses to those observed in miR166 mutants. We characterized increased transcription of AGO1 in response to infection with both ZYMV strains. Differences in viral siRNA profiles and accumulation between mild and severe virus infections were characterized by Illumina sequencing, probably due to the differences in HC-Pro binding activity. We determined that the TuMV FINK mutant could accumulate and cause symptoms in dcl2 dcl4 or dcl2 dcl3 dcl4 mutants similar to TuMV FRNK in wild type Arabidopsis plants. These dcl mutant plants are defective in antiviral defenses, and the results show that factors other than HC-ProFRNK motif can induce symptoms in virus-infected plants. As a result of this work, we have a better understanding of the FRNK and FKNH amino acid motifs of HC-Pro and their contributions to the duplex-siRNA binding functions. We have identified plant genes that potentially contribute to infectivity and symptoms of virus infected plants when they are mis-expressed during potyviral infections. The results establish that there are multiple underlying molecular mechanisms that lead viral pathogenicity, some dependent on HC-Pro. The potential benefits include the development of novel strategies for controlling diseases caused by viruses, methods to ensure stable expression of transgenes in genetically improved crops, and improved potyvirus vectors for expression of proteins or peptides in plants.
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Rafaeli, Ada, i Russell Jurenka. Molecular Characterization of PBAN G-protein Coupled Receptors in Moth Pest Species: Design of Antagonists. United States Department of Agriculture, grudzień 2012. http://dx.doi.org/10.32747/2012.7593390.bard.

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The proposed research was directed at determining the activation/binding domains and gene regulation of the PBAN-R’s thereby providing information for the design and screening of potential PBAN-R-blockers and to indicate possible ways of preventing the process from proceeding to its completion. Our specific aims included: (1) The identification of the PBAN-R binding domain by a combination of: (a) in silico modeling studies for identifying specific amino-acid side chains that are likely to be involved in binding PBAN with the receptor and; (b) bioassays to verify the modeling studies using mutant receptors, cell lines and pheromone glands (at tissue and organism levels) against selected, designed compounds to confirm if compounds are agonists or antagonists. (2) The elucidation ofthemolecular regulationmechanisms of PBAN-R by:(a) age-dependence of gene expression; (b) the effect of hormones and; (c) PBAN-R characterization in male hair-pencil complexes. Background to the topic Insects have several closely related G protein-coupled receptors (GPCRs) belonging to the pyrokinin/PBAN family, one with the ligand pheromone biosynthesis activating neuropeptide or pyrokinin-2 and another with diapause hormone or pyrokinin-1 as a ligand. We were unable to identify the diapause hormone receptor from Helicoverpa zea despite considerable effort. A third, related receptor is activated by a product of the capa gene, periviscerokinins. The pyrokinin/PBAN family of GPCRs and their ligands has been identified in various insects, such as Drosophila, several moth species, mosquitoes, Triboliumcastaneum, Apis mellifera, Nasoniavitripennis, and Acyrthosiphon pisum. Physiological functions of pyrokinin peptides include muscle contraction, whereas PBAN regulates pheromone production in moths plus other functions indicating the pleiotropic nature of these ligands. Based on the alignment of annotated genomic sequences, the primary and secondary structures of the pyrokinin/PBAN family of receptors have similarity with the corresponding structures of the capa or periviscerokinin receptors of insects and the neuromedin U receptors found in vertebrates. Major conclusions, solutions, achievements Evolutionary trace analysisof receptor extracellular domains exhibited several class-specific amino acid residues, which could indicate putative domains for activation of these receptors by ligand recognition and binding. Through site-directed point mutations, the 3rd extracellular domain of PBAN-R was shown to be critical for ligand selection. We identified three receptors that belong to the PBAN family of GPCRs and a partial sequence for the periviscerokinin receptor from the European corn borer, Ostrinianubilalis. Functional expression studies confirmed that only the C-variant of the PBAN-R is active. We identified a non-peptide agonist that will activate the PBAN-receptor from H. zea. We determined that there is transcriptional control of the PBAN-R in two moth species during the development of the pupa to adult, and we demonstrated that this transcriptional regulation is independent of juvenile hormone biosynthesis. This transcriptional control also occurs in male hair-pencil gland complexes of both moth species indicating a regulatory role for PBAN in males. Ultimate confirmation for PBAN's function in the male tissue was revealed through knockdown of the PBAN-R using RNAi-mediated gene-silencing. Implications, both scientific and agricultural The identification of a non-peptide agonist can be exploited in the future for the design of additional compounds that will activate the receptor and to elucidate the binding properties of this receptor. The increase in expression levels of the PBAN-R transcript was delineated to occur at a critical period of 5 hours post-eclosion and its regulation can now be studied. The mysterious role of PBAN in the males was elucidated by using a combination of physiological, biochemical and molecular genetics techniques.
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