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Journal articles on the topic 'Post-transcriptional gene regulation'

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Author: Grafiati

Published: 4 June 2021

Last updated: 21 February 2023

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1

Tew, Simon R., and Peter D. Clegg. "Post-transcriptional gene regulation in chondrocytes." Biochemical Society Transactions 38, no. 6 (November 24, 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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2

Lipshitz, Howard D., Julie M. Claycomb, and Craig A. Smibert. "Post-transcriptional regulation of gene expression." Methods 126 (August 2017): 1–2. http://dx.doi.org/10.1016/j.ymeth.2017.08.007.

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3

Kashanchi, Fatah, and John N. Brady. "Transcriptional and post-transcriptional gene regulation of HTLV-1." Oncogene 24, no. 39 (September 2005): 5938–51. http://dx.doi.org/10.1038/sj.onc.1208973.

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4

Alonso, C. R. "Post-transcriptional gene regulation via RNA control." Briefings in Functional Genomics 12, no. 1 (January 1, 2013): 1–2. http://dx.doi.org/10.1093/bfgp/els060.

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5

Zhao, Boxuan Simen, Ian A. Roundtree, and Chuan He. "Post-transcriptional gene regulation by mRNA modifications." Nature Reviews Molecular Cell Biology 18, no. 1 (November 3, 2016): 31–42. http://dx.doi.org/10.1038/nrm.2016.132.

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6

Swaminathan, Sankar. "Post-transcriptional gene regulation by gamma herpesviruses." Journal of Cellular Biochemistry 95, no. 4 (2005): 698–711. http://dx.doi.org/10.1002/jcb.20465.

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7

Sadelain, Michel. "Transcriptional and post transcriptional gene regulation in stem cell-based gene therapy." Blood Cells, Molecules, and Diseases 40, no. 2 (March 2008): 283. http://dx.doi.org/10.1016/j.bcmd.2007.10.074.

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8

Kuhlemier, Cris. "Transcriptional and post-transcriptional regulation of gene expression in plants." Plant Molecular Biology 19, no. 1 (May 1992): 1–14. http://dx.doi.org/10.1007/bf00015603.

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9

Ray, Swagat, Pól Ó. Catnaigh, and Emma C. Anderson. "Post-transcriptional regulation of gene expression by Unr." Biochemical Society Transactions 43, no. 3 (June 1, 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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10

Sánchez-Jiménez, Flora, and Víctor Sánchez-Margalet. "Role of Sam68 in Post-Transcriptional Gene Regulation." International Journal of Molecular Sciences 14, no. 12 (November 28, 2013): 23402–19. http://dx.doi.org/10.3390/ijms141223402.

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11

Boyne, J. R., and A. Whitehouse. "γ-2 herpes virus post-transcriptional gene regulation." Clinical Microbiology and Infection 12, no. 2 (February 2006): 110–17. http://dx.doi.org/10.1111/j.1469-0691.2005.01317.x.

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12

Klausner, R., and J. Harford. "cis-trans models for post-transcriptional gene regulation." Science 246, no. 4932 (November 17, 1989): 870–72. http://dx.doi.org/10.1126/science.2683086.

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13

Borden, K., B. Culjkovic, and S. Vukosavic. "eIF4E and post-transcriptional gene regulation in cancer." European Journal of Cancer Supplements 6, no. 9 (July 2008): 2. http://dx.doi.org/10.1016/s1359-6349(08)71182-0.

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14

Glisovic, Tina, Jennifer L. Bachorik, Jeongsik Yong, and Gideon Dreyfuss. "RNA-binding proteins and post-transcriptional gene regulation." FEBS Letters 582, no. 14 (March 13, 2008): 1977–86. http://dx.doi.org/10.1016/j.febslet.2008.03.004.

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15

Fujiwara, Shinsuke, and A. M. Chakrabarty. "Post-transcriptional regulation of the Pseudomonas aeruginosaalgC gene." Gene 146, no. 1 (August 1994): 1–5. http://dx.doi.org/10.1016/0378-1119(94)90826-5.

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16

Roger, T., X. Ding, A. L. Chanson, P. Renner, and T. Calandra. "84 Transcriptional and post-transcriptional regulation of human MIF gene expression." International Journal of Infectious Diseases 10 (2006): S47—S48. http://dx.doi.org/10.1016/s1201-9712(06)80081-0.

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17

Dykes, Iain M., and Costanza Emanueli. "Transcriptional and Post-transcriptional Gene Regulation by Long Non-coding RNA." Genomics, Proteomics & Bioinformatics 15, no. 3 (June 2017): 177–86. http://dx.doi.org/10.1016/j.gpb.2016.12.005.

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18

Fenton, Matthew J. "Review: Transcriptional and post-transcriptional regulation of interleukin 1 gene expression." International Journal of Immunopharmacology 14, no. 3 (April 1992): 401–11. http://dx.doi.org/10.1016/0192-0561(92)90170-p.

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19

Distel, R. J., G. S. Robinson, and B. M. Spiegelman. "Fatty acid regulation of gene expression. Transcriptional and post-transcriptional mechanisms." Journal of Biological Chemistry 267, no. 9 (March 1992): 5937–41. http://dx.doi.org/10.1016/s0021-9258(18)42645-2.

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20

Sankaran, Vijay G. "Post-Transcriptional Defects and Erythroid Pathobiology." Blood 124, no. 21 (December 6, 2014): SCI—35—SCI—35. http://dx.doi.org/10.1182/blood.v124.21.sci-35.sci-35.

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A great body of work has focused on understanding the role that gene regulation at the transcriptional level plays in blood cell production and diseases that disrupt this process. However, until recently there has been limited insight on the role that post-transcriptional gene regulation has in both normal and pathological disorders of human hematopoiesis. Specifically, the regulation of messenger RNA translation can have a significant impact upon gene expression, and how this process affects hematopoiesis has only been explored in limited studies. In this talk, the role of ribosomal protein gene mutations in the specific disorder of red blood cell production, Diamond-Blackfan anemia, will be discussed. Recent findings from our laboratory show that mutations in the key hematopoietic transcription factor gene, GATA1, can result in Diamond-Blackfan anemia in rare cases. We have gone on to show that more common mutations in ribosomal protein genes can disrupt translation of GATA1 and thereby suggest a common underlying mechanism for the impaired erythropoiesis observed in Diamond-Blackfan anemia. We discuss both the mechanistic underpinnings of our observations and how these findings have important therapeutic implications. Other recent examples of how disordered translation can impair human hematopoiesis will also be examined. This talk will provide a cohesive framework to understand the implications of these recent findings for both normal and disordered human hematopoiesis. Disclosures No relevant conflicts of interest to declare.

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21

Witzel, Ini-Isabée, Li Fang Koh, and Neil D. Perkins. "Regulation of cyclin D1 gene expression." Biochemical Society Transactions 38, no. 1 (January 19, 2010): 217–22. http://dx.doi.org/10.1042/bst0380217.

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Cyclin D1 is a key regulator of cell proliferation and its expression is subject to both transcriptional and post-transcriptional regulation. In different cellular contexts, different pathways assume a dominant role in regulating its expression, whereas their disregulation can contribute to overexpression of cyclin D1 in tumorigenesis. Here, we discuss the ability of the NF-κB (nuclear factor κB)/IKK [IκB (inhibitor of NF-κB) kinase] pathways to regulate cyclin D1 gene transcription and also consider the newly discovered role of the SNARP (SNIP1/SkIP-associated RNA processing) complex as a co-transcriptional regulator of cyclin D1 RNA stability.

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22

Liu, Meilian, and Feng Liu. "Transcriptional and post-translational regulation of adiponectin." Biochemical Journal 425, no. 1 (December 14, 2009): 41–52. http://dx.doi.org/10.1042/bj20091045.

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Adiponectin is an adipose-tissue-derived hormone with anti-diabetic, anti-atherogenic and anti-inflammatory functions. Adiponectin circulates in the bloodstream in trimeric, hexameric and high-molecular-mass species, and different forms of adiponectin have been found to play distinct roles in the regulation of energy homoeostasis. The serum levels of adiponectin are negatively correlated with obesity and insulin resistance, yet the underlying mechanisms remain elusive. In the present review, we summarize recent progress made on the mechanisms regulating adiponectin gene transcription, multimerization and secretion. We also discuss the potential relevance of these studies to the development of new clinical therapy for insulin resistance, Type 2 diabetes and other obesity-related metabolic disorders.

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23

van Grinsven, M. Q. J. M., J. J. L. Gielen, J. L. A. Zethof, H. J. J. Nijkamp, and A. J. Kool. "Transcriptional and post-transcriptional regulation of chloroplast gene expression in Petunia hybrida." Theoretical and Applied Genetics 73, no. 1 (November 1986): 94–101. http://dx.doi.org/10.1007/bf00273725.

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24

Anderson, C. J., S. F. Hoare, M. Ashcroft, A. E. Bilsland, and W. N. Keith. "Hypoxic regulation of telomerase gene expression by transcriptional and post-transcriptional mechanisms." Oncogene 25, no. 1 (September 19, 2005): 61–69. http://dx.doi.org/10.1038/sj.onc.1209011.

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25

Kula, Anna, and Alessandro Marcello. "Dynamic Post-Transcriptional Regulation of HIV-1 Gene Expression." Biology 1, no. 2 (July 3, 2012): 116–33. http://dx.doi.org/10.3390/biology1020116.

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26

Ellis, Tannis J., and Graham F. Wagner. "Post-transcriptional Regulation of the Stanniocalcin Gene by Calcium." Journal of Biological Chemistry 270, no. 4 (January 27, 1995): 1960–65. http://dx.doi.org/10.1074/jbc.270.4.1960.

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27

Yue, Yanan, Jianzhao Liu, and Chuan He. "RNAN6-methyladenosine methylation in post-transcriptional gene expression regulation." Genes & Development 29, no. 13 (July 1, 2015): 1343–55. http://dx.doi.org/10.1101/gad.262766.115.

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28

Khanin, Raya, and Veronica Vinciotti. "Computational Modeling of Post-Transcriptional Gene Regulation by MicroRNAs." Journal of Computational Biology 15, no. 3 (April 2008): 305–16. http://dx.doi.org/10.1089/cmb.2007.0184.

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29

CLERCH, LINDA BIADASZ. "Post-Transcriptional Regulation of Lung Antioxidant Enzyme Gene Expression." Annals of the New York Academy of Sciences 899, no. 1 (January 25, 2006): 103–11. http://dx.doi.org/10.1111/j.1749-6632.2000.tb06179.x.

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30

McKay, Bruce C. "Post-Transcriptional Regulation of DNA Damage-Responsive Gene Expression." Antioxidants & Redox Signaling 20, no. 4 (February 2014): 640–54. http://dx.doi.org/10.1089/ars.2013.5523.

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31

Peffers, M. J., R. Fentom, S. R. Tew, and P. D. Clegg. "Post transcriptional gene regulation in ageing cartilage and chondrocytes." Osteoarthritis and Cartilage 22 (April 2014): S62—S63. http://dx.doi.org/10.1016/j.joca.2014.02.128.

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32

Neil, Christopher R., and William G. Fairbrother. "Intronic RNA: Ad‘junk’ mediator of post-transcriptional gene regulation." Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms 1862, no. 11-12 (November 2019): 194439. http://dx.doi.org/10.1016/j.bbagrm.2019.194439.

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33

Goldie, Belinda J., and Murray J. Cairns. "Post-Transcriptional Trafficking and Regulation of Neuronal Gene Expression." Molecular Neurobiology 45, no. 1 (December 14, 2011): 99–108. http://dx.doi.org/10.1007/s12035-011-8222-0.

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34

Nishizawa, Mikio. "Post-transcriptional inducible gene regulation by natural antisense RNA." Frontiers in Bioscience 20, no. 1 (2015): 1–36. http://dx.doi.org/10.2741/4297.

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35

Zhao, Boxuan Simen, Ian A. Roundtree, and Chuan He. "Publisher Correction: Post-transcriptional gene regulation by mRNA modifications." Nature Reviews Molecular Cell Biology 19, no. 12 (October 19, 2018): 808. http://dx.doi.org/10.1038/s41580-018-0075-1.

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36

Carpenter, Susan, Emiliano P. Ricci, Blandine C. Mercier, Melissa J. Moore, and Katherine A. Fitzgerald. "Post-transcriptional regulation of gene expression in innate immunity." Nature Reviews Immunology 14, no. 6 (May 23, 2014): 361–76. http://dx.doi.org/10.1038/nri3682.

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37

Corbett, Anita H. "Post-transcriptional regulation of gene expression and human disease." Current Opinion in Cell Biology 52 (June 2018): 96–104. http://dx.doi.org/10.1016/j.ceb.2018.02.011.

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38

Akker, SA, PJ Smith, and SL Chew. "Nuclear post-transcriptional control of gene expression." Journal of Molecular Endocrinology 27, no. 2 (October 1, 2001): 123–31. http://dx.doi.org/10.1677/jme.0.0270123.

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The mammalian nucleus has considerable control over nascent transcripts. The basic mechanisms of post-transcriptional processing are well understood and recently some of the principles underlying the regulation of nuclear processing events have been elucidated. Here we review the recent progress in identification of signalling pathways that modulate the action of key RNA-binding proteins which regulate splicing, and the mechanisms of action of the C-terminal domain of RNA polymerase II that co-ordinate transcription with nuclear mRNA processing events.

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39

Swaminathan, Sanjay, Chantelle L. Hood, Kazuo Suzuki, and Anthony D. Kelleher. "RNA duplexes in transcriptional regulation." BioMolecular Concepts 1, no. 3-4 (October 1, 2010): 285–96. http://dx.doi.org/10.1515/bmc.2010.021.

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AbstractTranscriptional regulation by small RNA molecules, including small interfering RNA and microRNA, has emerged as an important gene expression modulator. The regulatory pathways controlling gene expression, post-transcriptional gene silencing and transcriptional gene silencing (TGS) have been demonstrated in yeast, plants and more recently in human cells. In this review, we discuss the currents models of transcriptional regulation and the main components of the RNA-induced silencing complex and RNA-induced transcriptional silencing complex machinery, as well as confounding off-target effects and gene activation. We also discuss RNA-mediated TGS within the NF-κB motif of the human immunodeficiency virus type 1 5′ long tandem repeat promoter region and the associated epigenetic modifications. Finally, we outline the current RNA interference (RNAi) delivery methods and describe the current status of human trials investigating potential RNAi therapeutics for several human diseases.

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40

Rosa, F. M., and M. Fellous. "Regulation of HLA-DR gene by IFN-gamma. Transcriptional and post-transcriptional control." Journal of Immunology 140, no. 5 (March 1, 1988): 1660–64. http://dx.doi.org/10.4049/jimmunol.140.5.1660.

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Abstract IFN-gamma increases the synthesis and level of mRNA of the HLA class I and II genes, in human cells such as melanomas which normally express both classes of molecules. It also induces the surface expression and mRNA synthesis of HLA-DR genes on cells which normally do not express HLA class II genes such as skin fibroblasts. We have investigated the mechanism by which IFN-gamma increases mRNA levels for class II MHC antigens in human cells. For this purpose, we have studied the effect of IFN-gamma on HLA-DR-alpha transcription rate in two different human cell types: VAL melanoma and JDA2 skin fibroblasts. HLA-DR-alpha mRNA is spontaneously produced in VAL cells and its level is enhanced upon IFN-gamma treatment. We demonstrate here that IFN-gamma increases the transcription of HLA-DR-alpha gene in this cell line. However, the discrepancy observed between HLA-DR-alpha mRNA and transcriptional rates led us to postulate that IFN-gamma also regulates the HLA-DR-alpha gene post-transcriptionally. In the course of these experiments, we found also that human skin fibroblasts, which do not contain detectable amounts of HLA-DR-alpha mRNA, spontaneously transcribe the HLA-DR-alpha gene.

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41

Vyas, S., N. Faucon Biguet, and J. Mallet. "Transcriptional and post-transcriptional regulation of tyrosine hydroxylase gene by protein kinase C." EMBO Journal 9, no. 11 (November 1990): 3707–12. http://dx.doi.org/10.1002/j.1460-2075.1990.tb07583.x.

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42

M, Hitit. "Putative Role of Micro - RNA s i n Female Reproductive Tract." Open Access Journal of Veterinary Science & Research 2, no. 2 (2017): 1–5. http://dx.doi.org/10.23880/oajvsr-16000131.

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Female reproductive tract is composed of ovarium, oviduct, cervix and uterus. Development and function of reproductive tract is dispens a ble for maintenance and achievement of reproduction. Reproductive tract responses to cyclic changes and ovarium hormones which provide optimum conditions for gam e t e movement and development. While the potential influence of pitu i tary and gonadal hormones on reproductive function is clearly understood, the molecular mechanism regulating reproductive tract remains elusive. Although, post - transcriptional gene regulation has critical role in cell differ e ntiation and proliferation, little information is ava i lable in post - transcriptional gene regulation in reproductive tract. Post - transcriptional g ene regulation includes splicing, processing, transport and translation of mRNA. In addition, role of RNA binding proteins and recently discovered miRNAs were also implicated in reproductive tract.

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43

Day, DA, and MF Tuite. "Post-transcriptional gene regulatory mechanisms in eukaryotes: an overview." Journal of Endocrinology 157, no. 3 (June 1, 1998): 361–71. http://dx.doi.org/10.1677/joe.0.1570361.

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Expression of a gene can be controlled at many levels, including transcription, mRNA splicing, mRNA stability, translation and post-translational events such as protein stability and modification. The majority of studies to date have focused on transcriptional control mechanisms, but the importance of post-transcriptional mechanisms in regulating gene expression in eukaryotes is becoming increasingly clear. In this short review, selected examples of post-transcriptional gene regulatory mechanisms operating in both lower and higher eukaryotes will be used to highlight the plethora of such mechanisms already identified. The underlying theme is that post-transcriptional gene regulation relies on specific RNA-protein interactions that either result in the targeted degradation of the mRNA or prevent access of the ribosome to the translation start codon. Such interactions can occur in the 5' or 3' untranslated regions of an mRNA or within the decoded portion of the molecule. The importance of these regulatory mechanisms in a range of biological systems is also illustrated.

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44

Aguilera, G., S. Volpi, and C. Rabadan-Diehl. "Transcriptional and post-transcriptional mechanisms regulating the rat pituitary vasopressin V1b receptor gene." Journal of Molecular Endocrinology 30, no. 2 (April 1, 2003): 99–108. http://dx.doi.org/10.1677/jme.0.0300099.

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The number of V1b vasopressin receptors (V1bR) in the anterior pituitary plays an important role during adaptation of the hypothalamic-pituitary-adrenal axis to stress in rats. Regulation of V1bR expression involves transcriptional and translational mechanisms. One of the elements mediating transcriptional activation of the rat V1bR gene is a long stretch of GAGA repeats (GAGA box) in the promoter located near the transcription start point capable of binding a protein complex of 127 kDa present in pituitary nuclear extracts. There is a lack of correlation between changes in V1bR mRNA and the number of VP binding sites, suggesting that V1bR expression depends on the efficiency of V1b R mRNA translation into protein. Two mechanisms by which the 5' untranslated region (5'-UTR) of the rat V1bR mRNA can mediate either inhibition or activation of V1bR mRNA translation have been identified. First, upstream open reading frames (ORF) present in the 5'-UTR repress translation of the major ORF encoding the V1b receptor, and secondly, an internal ribosome entry site (IRES) activates V1bR translation. Stimulation of IRES activity through protein kinase C-mediated pathways results in V1bR mRNA translation increasing V1bR protein levels. The existence of multiple loci of regulation for the V1bR at transcriptional and translational levels provides a mechanism to facilitate plasticity of regulation of the number of pituitary vasopressin receptors according to physiological demand.

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45

Laloo, Benoît, Marion Maurel, Sandra Jalvy-Delvaille, Francis Sagliocco, and Christophe F. Grosset. "Analysis of post-transcriptional regulation using the FunREG method." Biochemical Society Transactions 38, no. 6 (November 24, 2010): 1608–14. http://dx.doi.org/10.1042/bst0381608.

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An increasing number of arguments, including altered microRNA expression, support the idea that post-transcriptional deregulation participates in gene disturbances found in diseased tissues. To evaluate this hypothesis, we developed a method which facilitates post-transcriptional investigations in a wide range of human cells and experimental conditions. This method, called FunREG (functional, integrated and quantitative method to measure post-transcriptional regulation), connects lentiviral transduction with a fluorescent reporter system and quantitative PCR. Using FunREG, we efficiently measured post-transcriptional regulation mediated either by selected RNA sequences or regulatory factors (microRNAs), and then evaluated the contribution of mRNA decay and translation efficiency in the observed regulation. We demonstrated the existence of gene-specific post-transcriptional deregulation in liver tumour cells, and also reported a molecular link between a transcript variant abrogating HDAC6 (histone deacetylase 6) regulation by miR-433 and a rare familial genetic disease. Because FunREG is sensitive, quantitative and easy to use, many applications can be envisioned in fundamental and pathophysiological research.

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46

De Gaudenzi, Javier G., Griselda Noé, Vanina A. Campo, Alberto C. Frasch, and Alejandro Cassola. "Gene expression regulation in trypanosomatids." Essays in Biochemistry 51 (October 24, 2011): 31–46. http://dx.doi.org/10.1042/bse0510031.

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Trypanosomatids are protozoan micro-organisms that cause serious health problems in humans and domestic animals. In addition to their medical relevance, these pathogens have novel biological structures and processes. From nuclear DNA transcription to mRNA translation, trypanosomes use unusual mechanisms to control gene expression. For example, transcription by RNAPII (RNA polymerase II) is polycistronic, and only a few transcription initiation sites have been identified so far. The sequences present in the polycistronic units code for proteins having unrelated functions, that is, not involved in a similar metabolic pathway. Owing to these biological constraints, these micro-organisms regulate gene expression mostly by post-transcriptional events. Consequently, the function of proteins that recognize RNA elements preferentially at the 3′ UTR (untranslated region) of transcripts is central. It was recently shown that mRNP (messenger ribonucleoprotein) complexes are organized within post-transcriptional operons to co-ordinately regulate gene expression of functionally linked transcripts. In the present chapter we will focus on particular characteristics of gene expression in the so-called TriTryp parasites: Trypanosoma cruzi, Trypanosoma brucei and Leishmania major.

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47

Martínez-Andújar, C., R. C. Martin, G. W. Bassel, M. B. Arun Kumar, W. E. Pluskota, and H. Nonogaki. "POST-TRANSCRIPTIONAL GENE REGULATION DURING SEED GERMINATION AND STAND ESTABLISHMENT." Acta Horticulturae, no. 898 (June 2011): 53–59. http://dx.doi.org/10.17660/actahortic.2011.898.5.

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48

Ghanekar, Yashoda, and Subhashini Sadasivam. "RNA Editing–Associated Post-Transcriptional Gene Regulation in Rheumatoid Arthritis." Bioinformatics and Biology Insights 16 (January 2022): 117793222210887. http://dx.doi.org/10.1177/11779322221088725.

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Background: Rheumatoid arthritis (RA) is an autoimmune disease characterised by systemic inflammation of joints. The observed complexity of RA pathogenesis and studies that have been carried out so far indicate that RA pathogenesis is regulated at multiple levels. Given the role of RNA editing in autoimmune disease, we hypothesised that RNA editing could contribute to RA pathogenesis by regulating gene expression through post-transcriptional mechanisms. Methods: We identified RNA editing events in synovial tissues from early and established RA compared with normal subjects from an available transcriptome data set using REDItools. To investigate the potential effect of these RNA editing events on gene expression, we carried out an analysis of differential exon usage in the vicinity of the differentially edited sites using DEXSeq. We then used STRING to identify putative interactions between differentially edited genes identified from REDItools analysis. We also investigated the possible effects of these RNA editing events on miRNA-target mRNA interactions as predicted by miRanda. Results: Our analysis revealed that there is extensive RNA editing in RA, with 304 and 273 differentially edited events in early RA and established RA, respectively. Of these, 25 sites were within 11 genes in early RA, and 34 sites were within 7 genes in established RA. DEXSeq analysis revealed that RNA editing correlated with differential exon usage in 4 differentially edited genes that have previously also been associated with RA in some measure: ATM, ZEB1, ANXA4, and TIMP3. DEXSeq analysis also revealed enrichment of some non-functional isoforms of these genes, perhaps at the expense of their full-length counterparts. Network analysis using STRING showed that several edited genes were part of the p53 protein-protein interaction network. We also identified several putative miRNA binding sites in the differentially edited genes that were lost upon editing. Conclusions: Our results suggested that the expression of genes involved in DNA repair and cell cycle, including ATM and ZEB1 which are well-known functional regulators of the DNA damage response pathway, could be regulated by RNA editing in RA synovia. This may contribute to an impaired DNA damage response in synovial tissues.

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49

McFadden, Michael J., Alexa B. R. McIntyre, Haralambos Mourelatos, Nathan S. Abell, Nandan S. Gokhale, Hélène Ipas, Blerta Xhemalçe, Christopher E. Mason, and Stacy M. Horner. "Post-transcriptional regulation of antiviral gene expression by N6-methyladenosine." Cell Reports 34, no. 9 (March 2021): 108798. http://dx.doi.org/10.1016/j.celrep.2021.108798.

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50

Tomasoni, Susanna, and Ariela Benigni. "Post-Transcriptional Gene Regulation Makes Things Clearer in Renal Fibrosis." Journal of the American Society of Nephrology 24, no. 7 (May 30, 2013): 1026–28. http://dx.doi.org/10.1681/asn.2013040411.

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