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Journal articles on the topic 'Intronic polyadenylation'

Author: Grafiati

Published: 25 May 2024

Last updated: 31 July 2025

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1

Tikhonov, M. V., P. G. Georgiev, and O. G. Maksimenko. "Competition within Introns: Splicing Wins over Polyadenylation via a General Mechanism." Acta Naturae 5, no. 4 (2013): 52–61. http://dx.doi.org/10.32607/20758251-2013-5-4-52-61.

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Most eukaryotic messenger RNAs are capped, spliced, and polyadenylated via co-transcriptional processes that are coupled to each other and to the transcription machinery. Coordination of these processes ensures correct RNA maturation and provides for the diversity of the transcribed isoforms. Thus, RNA processing is a chain of events in which the completion of one event is coupled to the initiation of the next one. In this context, the relationship between splicing and polyadenylation is an important aspect of gene regulation. We have found that cryptic polyadenylation signals are widely distr

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Wang, Xiuye, Liang Liu, Adam W. Whisnant, et al. "Mechanism and consequences of herpes simplex virus 1-mediated regulation of host mRNA alternative polyadenylation." PLOS Genetics 17, no. 3 (2021): e1009263. http://dx.doi.org/10.1371/journal.pgen.1009263.

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Eukaryotic gene expression is extensively regulated by cellular stress and pathogen infections. We have previously shown that herpes simplex virus 1 (HSV-1) and several cellular stresses cause widespread disruption of transcription termination (DoTT) of RNA polymerase II (RNAPII) in host genes and that the viral immediate early factor ICP27 plays an important role in HSV-1-induced DoTT. Here, we show that HSV-1 infection also leads to widespread changes in alternative polyadenylation (APA) of host mRNAs. In the majority of cases, polyadenylation shifts to upstream poly(A) sites (PAS), includin

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3

Lou, Hua, Karla M. Neugebauer, Robert F. Gagel, and Susan M. Berget. "Regulation of Alternative Polyadenylation by U1 snRNPs and SRp20." Molecular and Cellular Biology 18, no. 9 (1998): 4977–85. http://dx.doi.org/10.1128/mcb.18.9.4977.

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ABSTRACT Although considerable information is currently available about the factors involved in constitutive vertebrate polyadenylation, the factors and mechanisms involved in facilitating communication between polyadenylation and splicing are largely unknown. Even less is known about the regulation of polyadenylation in genes in which 3′-terminal exons are alternatively recognized. Here we demonstrate that an SR protein, SRp20, affects recognition of an alternative 3′-terminal exon via an effect on the efficiency of binding of a polyadenylation factor to an alternative polyadenylation site. T

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4

Spraggon, Lee, and Luca Cartegni. "U1 snRNP-Dependent Suppression of Polyadenylation: Physiological Role and Therapeutic Opportunities in Cancer." International Journal of Cell Biology 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/846510.

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Pre-mRNA splicing and polyadenylation are critical steps in the maturation of eukaryotic mRNA. U1 snRNP is an essential component of the splicing machinery and participates in splice-site selection and spliceosome assembly by base-pairing to the 5′ splice site. U1 snRNP also plays an additional, nonsplicing global function in 3′ end mRNA processing; it actively suppresses the polyadenylation machinery from using early, mostly intronic polyadenylation signals which would lead to aberrant, truncated mRNAs. Thus, U1 snRNP safeguards pre-mRNA transcripts against premature polyadenylation and contr

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Scholl, Amanda, Alexander Muselman, and Dong-Er Zhang. "An Intronic Suppressor Element Regulates RUNX1 Alternative Polyadenylation." Blood 126, no. 23 (2015): 3578. http://dx.doi.org/10.1182/blood.v126.23.3578.3578.

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Abstract Polyadenylation is a post-transcriptional modification where the 3' end of an mRNA is cleaved and 250-300 adenines are added. It is predicted that 70-75% of human genes have more than one polyadenylation sequence (PAS) and are subject to alternative polyadenylation (APA). APA events affect the coding sequence of a gene when a proximal PAS is located within an intron, constitutive exon, or alternative exon. Gene expression is also affected if there are multiple PAS within the distal 3' untranslated region (UTR); proximal PAS usage shortens the 3'UTR, which can remove cis-regulatory reg

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6

Duan, Cheng-Guo, Xingang Wang, Lingrui Zhang, et al. "A protein complex regulates RNA processing of intronic heterochromatin-containing genes in Arabidopsis." Proceedings of the National Academy of Sciences 114, no. 35 (2017): E7377—E7384. http://dx.doi.org/10.1073/pnas.1710683114.

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In several eukaryotic organisms, heterochromatin (HC) in the introns of genes can regulate RNA processing, including polyadenylation, but the mechanism underlying this regulation is poorly understood. By promoting distal polyadenylation, the bromo-adjacent homology (BAH) domain-containing and RNA recognition motif-containing protein ASI1 and the H3K9me2-binding protein EDM2 are required for the expression of functional full-length transcripts of intronic HC-containing genes in Arabidopsis. Here we report that ASI1 and EDM2 form a protein complex in vivo via a bridge protein, ASI1-Immunoprecipi

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7

Wang, Ruijia, and Bin Tian. "APAlyzer: a bioinformatics package for analysis of alternative polyadenylation isoforms." Bioinformatics 36, no. 12 (2020): 3907–9. http://dx.doi.org/10.1093/bioinformatics/btaa266.

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Abstract Summary Most eukaryotic genes produce alternative polyadenylation (APA) isoforms. APA is dynamically regulated under different growth and differentiation conditions. Here, we present a bioinformatics package, named APAlyzer, for examining 3′UTR APA, intronic APA and gene expression changes using RNA-seq data and annotated polyadenylation sites in the PolyA_DB database. Using APAlyzer and data from the GTEx database, we present APA profiles across human tissues. Availability and implementation APAlyzer is freely available at https://bioconductor.org/packages/release/bioc/html/APAlyzer.

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8

Lee, Shih-Han, Irtisha Singh, Sarah Tisdale, Omar Abdel-Wahab, Christina S. Leslie, and Christine Mayr. "Widespread intronic polyadenylation inactivates tumour suppressor genes in leukaemia." Nature 561, no. 7721 (2018): 127–31. http://dx.doi.org/10.1038/s41586-018-0465-8.

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9

Dubbury, Sara J., Paul L. Boutz, and Phillip A. Sharp. "CDK12 regulates DNA repair genes by suppressing intronic polyadenylation." Nature 564, no. 7734 (2018): 141–45. http://dx.doi.org/10.1038/s41586-018-0758-y.

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10

Wang, Hong-Wei. "A Link between Intronic Polyadenylation and HR Maintenance Discovered." Biochemistry 58, no. 14 (2019): 1835–36. http://dx.doi.org/10.1021/acs.biochem.9b00202.

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11

Kan, J. "Intronic polyadenylation in the human glycinamide ribonucleotide formyltransferase gene." Nucleic Acids Research 25, no. 15 (1997): 3118–23. http://dx.doi.org/10.1093/nar/25.15.3118.

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12

Lepennetier, Gildas, and Francesco Catania. "Exploring the Impact of Cleavage and Polyadenylation Factors on Pre-mRNA Splicing Across Eukaryotes." G3 Genes|Genomes|Genetics 7, no. 7 (2017): 2107–14. http://dx.doi.org/10.1534/g3.117.041483.

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Abstract In human, mouse, and Drosophila, the spliceosomal complex U1 snRNP (U1) protects transcripts from premature cleavage and polyadenylation at proximal intronic polyadenylation signals (PAS). These U1-mediated effects preserve transcription integrity, and are known as telescripting. The watchtower role of U1 throughout transcription is clear. What is less clear is whether cleavage and polyadenylation factors (CPFs) are simply patrolled or if they might actively antagonize U1 recruitment. In addressing this question, we found that, in the introns of human, mouse, and Drosophila, and of 14

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13

Liu, Liang, Elizabeth Forbes, and Wei Zhang. "Abstract 5646: Altered intronic polyadenylation by mutant p53 impairs transcription of DNA repair genes in lung cancer." Cancer Research 84, no. 6_Supplement (2024): 5646. http://dx.doi.org/10.1158/1538-7445.am2024-5646.

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Abstract Introduction: Changes in alternative pre-mRNA processing have been found in many cancers. Aberrant intronic polyadenylation (IPA) causes a stop of normal transcription resulting in the production of truncated mRNA isoform or lncRNA. We sought to examine the role of mutant p53 in pre-mRNA processing, especially in IPA regulation in lung cancer. Methods: We established stable cell lines transfected with mutant p53 (R273H, R175H, H179Q, C238Y, and C242F) or vector control using the NSCLC cell line H1299 with a homozygous deletion of the endogenous p53. Total RNA was used to build librari

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14

Winstanley-Zarach, Phaedra, Gregor Rot, Shweta Kuba, Aibek Smagul, Mandy J. Peffers, and Simon R. Tew. "Analysis of RNA Polyadenylation in Healthy and Osteoarthritic Human Articular Cartilage." International Journal of Molecular Sciences 24, no. 7 (2023): 6611. http://dx.doi.org/10.3390/ijms24076611.

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Polyadenylation (polyA) defines the 3′ boundary of a transcript’s genetic information. Its position can vary and alternative polyadenylation (APA) transcripts can exist for a gene. This causes variance in 3′ regulatory domains and can affect coding sequence if intronic events occur. The distribution of polyA sites on articular chondrocyte transcripts has not been studied so we aimed to define their transcriptome-wide location in age-matched healthy and osteoarthritic knee articular cartilage. Total RNA was isolated from frozen tissue samples and analysed using the QuantSeq-Reverse 3′ RNA seque

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15

Rani, Abdul Qawee Mahyoob, Tetsushi Yamamoto, Tatsuya Kawaguchi, et al. "Intronic Alternative Polyadenylation in the Middle of the DMD Gene Produces Half-Size N-Terminal Dystrophin with a Potential Implication of ECG Abnormalities of DMD Patients." International Journal of Molecular Sciences 21, no. 10 (2020): 3555. http://dx.doi.org/10.3390/ijms21103555.

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The DMD gene is one of the largest human genes, being composed of 79 exons, and encodes dystrophin Dp427m which is deficient in Duchenne muscular dystrophy (DMD). In some DMD patient, however, small size dystrophin reacting with antibody to N-terminal but not to C-terminal has been identified. The mechanism to produce N-terminal small size dystrophin remains unknown. Intronic polyadenylation is a mechanism that produces a transcript with a new 3′ terminal exon and a C-terminal truncated protein. In this study, intronic alternative polyadenylation was disclosed to occur in the middle of the DMD

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16

Mueller, Alisa A., Cindy T. van Velthoven, Kathryn D. Fukumoto, Tom H. Cheung та Thomas A. Rando. "Intronic polyadenylation of PDGFRα in resident stem cells attenuates muscle fibrosis". Nature 540, № 7632 (2016): 276–79. http://dx.doi.org/10.1038/nature20160.

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17

Sommer, Jan, Christoph Garbers, Janina Wolf, et al. "Alternative Intronic Polyadenylation Generates the Interleukin-6 Trans-signaling Inhibitor sgp130-E10." Journal of Biological Chemistry 289, no. 32 (2014): 22140–50. http://dx.doi.org/10.1074/jbc.m114.560938.

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18

Wang, Ruijia, Dinghai Zheng, Lu Wei, Qingbao Ding, and Bin Tian. "Regulation of Intronic Polyadenylation by PCF11 Impacts mRNA Expression of Long Genes." Cell Reports 26, no. 10 (2019): 2766–78. http://dx.doi.org/10.1016/j.celrep.2019.02.049.

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19

Castelo-Branco, Pedro, Andre Furger, Matthew Wollerton, Christopher Smith, Alexandra Moreira, and Nick Proudfoot. "Polypyrimidine Tract Binding Protein Modulates Efficiency of Polyadenylation." Molecular and Cellular Biology 24, no. 10 (2004): 4174–83. http://dx.doi.org/10.1128/mcb.24.10.4174-4183.2004.

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ABSTRACT Polypyrimidine tract binding protein (PTB) is a major hnRNP protein with multiple roles in mRNA metabolism, including regulation of alternative splicing and internal ribosome entry site-driven translation. We show here that a fourfold overexpression of PTB results in a 75% reduction of mRNA levels produced from transfected gene constructs with different polyadenylation signals (pA signals). This effect is due to the reduced efficiency of mRNA 3′ end cleavage, and in vitro analysis reveals that PTB competes with CstF for recognition of the pA signal's pyrimidine-rich downstream sequenc

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20

Tian, Shuye, Bin Zhang, Yuhao He, et al. "CRISPR-iPAS: a novel dCAS13-based method for alternative polyadenylation interference." Nucleic Acids Research 50, no. 5 (2022): e26-e26. http://dx.doi.org/10.1093/nar/gkac108.

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Abstract Alternative polyadenylation (APA) plays an important role in gene regulation. With the recent application of novel sequencing technology in APA profiling, an ever-increasing number of APA genes/sites have been identified. However, the phenotypic relevance of most of these APA isoforms remains elusive, which is largely due to the lack of a convenient genetics tool for APA interference. To address this issue, herein, an efficient method is developed based on the CRISPR-dCas13 system, termed as CRISPR-iPAS. Out of eight different dCas13 proteins, Porphyromonas gulae (Pgu) dCas13b, is ide

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21

Elton, Terry S., Victor A. Hernandez, Jessika Carvajal-Moreno, Xinyi Wang, Deborah Ipinmoroti та Jack C. Yalowich. "Intronic Polyadenylation in Acquired Cancer Drug Resistance Circumvented by Utilizing CRISPR/Cas9 with Homology-Directed Repair: The Tale of Human DNA Topoisomerase IIα". Cancers 14, № 13 (2022): 3148. http://dx.doi.org/10.3390/cancers14133148.

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Intronic polyadenylation (IPA) plays a critical role in malignant transformation, development, progression, and cancer chemoresistance by contributing to transcriptome/proteome alterations. DNA topoisomerase IIα (170 kDa, TOP2α/170) is an established clinical target for anticancer agents whose efficacy is compromised by drug resistance often associated with a reduction of nuclear TOP2α/170 levels. In leukemia cell lines with acquired resistance to TOP2α-targeted drugs and reduced TOP2α/170 expression, variant TOP2α mRNA transcripts have been reported due to IPA that resulted in the translation

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22

Kaer, Kristel, Jelena Branovets, Anni Hallikma, Pilvi Nigumann, and Mart Speek. "Intronic L1 Retrotransposons and Nested Genes Cause Transcriptional Interference by Inducing Intron Retention, Exonization and Cryptic Polyadenylation." PLoS ONE 6, no. 10 (2011): e26099. http://dx.doi.org/10.1371/journal.pone.0026099.

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23

Druhan, Lawrence J., Amanda Lance, Alicia Hamilton, Nury M. Steuerwald, Elise Tjaden, and Belinda R. Avalos. "Alternative Splicing and Intronic Polyadenylation Post-Transcriptionally Regulate CSF3R Via a Cryptic Exon." Blood 134, Supplement_1 (2019): 2462. http://dx.doi.org/10.1182/blood-2019-129102.

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Increasing evidence suggests that alternative splicing of CSF3R occurs during normal granulopoiesis and is altered in certain pathologic conditions. To further examine CSF3R splicing, Sashimi plots from RNA-seq data were generated from CD34+ cells and neutrophils isolated from healthy donors (Figure 1A). The majority of splicing events were found to follow a pattern of enforced exon order resulting in production of CSF3R-V1, and to a lesser extent production of variants 3 and 4 that arise from alternative splicing of distal exonic sequences. However, a significant number of splicing events als

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Shulman, Eldad David, and Ran Elkon. "Cell-type-specific analysis of alternative polyadenylation using single-cell transcriptomics data." Nucleic Acids Research 47, no. 19 (2019): 10027–39. http://dx.doi.org/10.1093/nar/gkz781.

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AbstractAlternative polyadenylation (APA) is emerging as an important layer of gene regulation because the majority of mammalian protein-coding genes contain multiple polyadenylation (pA) sites in their 3′ UTR. By alteration of 3′ UTR length, APA can considerably affect post-transcriptional gene regulation. Yet, our understanding of APA remains rudimentary. Novel single-cell RNA sequencing (scRNA-seq) techniques allow molecular characterization of different cell types to an unprecedented degree. Notably, the most popular scRNA-seq protocols specifically sequence the 3′ end of transcripts. Buil

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Tsuchiya, T., and T. Eulgem. "An alternative polyadenylation mechanism coopted to the Arabidopsis RPP7 gene through intronic retrotransposon domestication." Proceedings of the National Academy of Sciences 110, no. 37 (2013): E3535—E3543. http://dx.doi.org/10.1073/pnas.1312545110.

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26

Gong, Qiuming, Matthew R. Stump, and Zhengfeng Zhou. "Upregulation of functional Kv11.1 isoform expression by inhibition of intronic polyadenylation with antisense morpholino oligonucleotides." Journal of Molecular and Cellular Cardiology 76 (November 2014): 26–32. http://dx.doi.org/10.1016/j.yjmcc.2014.08.007.

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27

Druhan, Lawrence J., Amanda Lance, Alicia Hamilton, Nury M. Steuerwald, Elise Tjaden, and Belinda R. Avalos. "Altered splicing and intronic polyadenylation of CSF3R via a cryptic exon in acute myeloid leukemia." Leukemia Research 92 (May 2020): 106349. http://dx.doi.org/10.1016/j.leukres.2020.106349.

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28

Winchester, Joni S., Eric C. Rouchka, Naomi S. Rowland, and Nancy A. Rice. "In Silico characterization of phosphorylase kinase: Evidence for an alternate intronic polyadenylation site in PHKG1." Molecular Genetics and Metabolism 92, no. 3 (2007): 234–42. http://dx.doi.org/10.1016/j.ymgme.2007.06.015.

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29

Feng, Qiumin, Zejin Lin, Danhui Zhao, et al. "Functional inhibition of core spliceosomal machinery activates intronic premature cleavage and polyadenylation of pre-mRNAs." Cell Reports 44, no. 3 (2025): 115376. https://doi.org/10.1016/j.celrep.2025.115376.

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Wang, Pingzhang, Peng Yu, Peng Gao, Taiping Shi, and Dalong Ma. "Discovery of novel human transcript variants by analysis of intronic single-block EST with polyadenylation site." BMC Genomics 10, no. 1 (2009): 518. http://dx.doi.org/10.1186/1471-2164-10-518.

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31

Pan, Zhenhua, Haibo Zhang, Lisa K. Hague, Ju Youn Lee, Carol S. Lutz, and Bin Tian. "An intronic polyadenylation site in human and mouse CstF-77 genes suggests an evolutionarily conserved regulatory mechanism." Gene 366, no. 2 (2006): 325–34. http://dx.doi.org/10.1016/j.gene.2005.09.024.

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32

Zhang, Ganggang, Bin Lan, Xin Zhang, et al. "AR-A014418 regulates intronic polyadenylation and transcription of PD-L1 through inhibiting CDK12 and CDK13 in tumor cells." Journal for ImmunoTherapy of Cancer 11, no. 5 (2023): e006483. http://dx.doi.org/10.1136/jitc-2022-006483.

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BackgroundImmune checkpoint molecules, especially programmed death 1 (PD-1) and its ligand, programmed death ligand 1 (PD-L1), protect tumor cells from T cell-mediated killing. Immune checkpoint inhibitors, designed to restore the antitumor immunosurveillance, have exhibited significant clinical benefits for patients with certain cancer types. Nevertheless, the relatively low response rate and acquisition of resistance greatly limit their clinical applications. A deeper understanding of the regulatory mechanisms of PD-L1 protein expression and activity will help to develop more effective thera

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Pawlicki, Jan M., and Joan A. Steitz. "Primary microRNA transcript retention at sites of transcription leads to enhanced microRNA production." Journal of Cell Biology 182, no. 1 (2008): 61–76. http://dx.doi.org/10.1083/jcb.200803111.

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MicroRNAs (miRNAs) are noncoding RNAs with important roles in regulating gene expression. In studying the earliest nuclear steps of miRNA biogenesis, we observe that primary miRNA (pri-miRNA) transcripts retained at transcription sites due to the deletion of 3′-end processing signals are converted more efficiently into precursor miRNAs (pre-miRNAs) than pri-miRNAs that are cleaved, polyadenylated, and released. Flanking exons, which also increase retention at transcription sites, likewise contribute to increased levels of intronic pri-miRNAs. Consistently, efficiently processed endogenous pri-

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Wu, Zhe, Robert Ietswaart, Fuquan Liu, Hongchun Yang, Martin Howard, and Caroline Dean. "Quantitative regulation of FLC via coordinated transcriptional initiation and elongation." Proceedings of the National Academy of Sciences 113, no. 1 (2015): 218–23. http://dx.doi.org/10.1073/pnas.1518369112.

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The basis of quantitative regulation of gene expression is still poorly understood. In Arabidopsis thaliana, quantitative variation in expression of FLOWERING LOCUS C (FLC) influences the timing of flowering. In ambient temperatures, FLC expression is quantitatively modulated by a chromatin silencing mechanism involving alternative polyadenylation of antisense transcripts. Investigation of this mechanism unexpectedly showed that RNA polymerase II (Pol II) occupancy changes at FLC did not reflect RNA fold changes. Mathematical modeling of these transcriptional dynamics predicted a tight coordin

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35

Urbanczyk, Andreas, Anselm Jünemann та Ralf Enz. "PKCζ-interacting protein ZIP3 is generated by intronic polyadenylation, and is expressed in the brain and retina of the rat". Biochemical Journal 433, № 1 (2010): 43–50. http://dx.doi.org/10.1042/bj20101111.

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Scaffold proteins contain multiple protein–protein interaction modules that physically assemble functionally related proteins into larger complexes. ZIPs [PKC (protein kinase C) ζ-interacting proteins] link the enzymatic activity of the atypical PKC isoforms PKCλ/ι or PKCζ to target proteins and are associated with neurodegenerative disorders. In the rat, alternative splicing generates three ZIP variants. Previously, we identified the ZIP3 transcript, containing 13 C-terminal amino acids encoded by intron 4, in the rat CNS (central nervous system). In the present study, we identified intronic

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Tellier, Michael, Gilbert Ansa, and Shona Murphy. "Isoginkgetin and Madrasin are poor splicing inhibitors." PLOS ONE 19, no. 10 (2024): e0310519. http://dx.doi.org/10.1371/journal.pone.0310519.

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The production of eukaryotic mRNAs requires transcription by RNA polymerase (pol) II and co-transcriptional processing, including capping, splicing, and cleavage and polyadenylation. Pol II can positively affect co-transcriptional processing through interaction of factors with its carboxyl terminal domain (CTD), comprising 52 repeats of the heptapeptide Tyr1-Ser2-Pro3-Thr4-Ser5-Pro6-Ser7, and pol II elongation rate can regulate splicing. Splicing, in turn, can also affect transcriptional activity and transcription elongation defects are caused by some splicing inhibitors. Multiple small molecu

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Kan, Julie L. C., and Richard G. Moran. "Analysis of a Mouse Gene Encoding Three Steps of Purine Synthesis Reveals Use of an Intronic Polyadenylation Signal without Alternative Exon Usage." Journal of Biological Chemistry 270, no. 4 (1995): 1823–32. http://dx.doi.org/10.1074/jbc.270.4.1823.

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Thomas, Christie P., Janet I. Andrews, and Kang Z. Liu. "Intronic polyadenylation signal sequences and alternate splicing generate human soluble Fltl variants and regulate the abundance of soluble Flt1 in the placenta." FASEB Journal 21, no. 14 (2007): 3885–95. http://dx.doi.org/10.1096/fj.07-8809com.

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Samur, Mehmet K., Irtisha Singh, Lee Shih-Han, et al. "3' Untranslated Region (UTR) Alterations Are Frequently Targeted By MM-Related Mirnas and Affects the Clinical Outcome." Blood 128, no. 22 (2016): 4447. http://dx.doi.org/10.1182/blood.v128.22.4447.4447.

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Abstract More than half of human genes use alternative cleavage and polyadenylation to generate alternative 3' untranslated region (3'UTR) isoforms that play a role in gene expression regulation. The 3' untranslated region (3'UTR) of mRNA contains elements that play regulatory roles in polyadenylation, localization, translation efficiency, and mRNA stability. Although relative contributions of different regulatory mechanisms remain poorly understood, several recent studies showed that alterations in 3'UTRs might affect protein localization as well as their interactions with other proteins. Her

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Thomas, Christie P., Nandita S. Raikwar, Elizabeth A. Kelley, and Kang Z. Liu. "Alternate processing of Flt1 transcripts is directed by conserved cis -elements within an intronic region of FLT1 that reciprocally regulates splicing and polyadenylation." Nucleic Acids Research 38, no. 15 (2010): 5130–40. http://dx.doi.org/10.1093/nar/gkq198.

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41

Zhao, Xinyu, Xinyi Wang, Sarah Eaton, Terry Elton, and Jack Yalowich. "Abrogation of Intronic Polyadenylation: CRISPR/Cas9-based Gene-editing to Circumvent Acquired Resistance to DNA Topoisomerase II-targeted Anticancer Agents (Abstract ID: 161640)." Journal of Pharmacology and Experimental Therapeutics 392, no. 3 (2025): 100550. https://doi.org/10.1016/j.jpet.2024.100550.

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Lian, Jin, Zheng Lian, Alexander Karpikov, et al. "Genomic Distribution of Transcripts and DNA Associated Proteins in One Percent of the Genome of Erythroid and Myeloid Cells." Blood 108, no. 11 (2006): 4201. http://dx.doi.org/10.1182/blood.v108.11.4201.4201.

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Abstract The NIHGRI has sponsored a multi-group enterprise to use a variety of approaches to map DNA elements in one per cent of the human genome-the ENCODE Project. As part of this effort we have mapped sites of active transcription (transcriptionally active regions or TARS) for myeloid cells including the undifferentiated and retinoic acid treated promyelocytic NB4 cell line and normal neutrophils, as well as the erythroid cell line K562. The results show a large number of intergenic and intronic transcripts, particularly in neutrophils. One feature of note is the amount of cell type specifi

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Luo, Wenting, Zhe Ji, Zhenhua Pan, et al. "The Conserved Intronic Cleavage and Polyadenylation Site of CstF-77 Gene Imparts Control of 3′ End Processing Activity through Feedback Autoregulation and by U1 snRNP." PLoS Genetics 9, no. 7 (2013): e1003613. http://dx.doi.org/10.1371/journal.pgen.1003613.

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Ganaie, Safder S., Aaron Yun Chen, Chun Huang, et al. "RNA Binding Protein RBM38 Regulates Expression of the 11-Kilodalton Protein of Parvovirus B19, Which Facilitates Viral DNA Replication." Journal of Virology 92, no. 8 (2018): e02050-17. http://dx.doi.org/10.1128/jvi.02050-17.

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ABSTRACTHuman parvovirus B19 (B19V) expresses a single precursor mRNA (pre-mRNA), which undergoes alternative splicing and alternative polyadenylation to generate 12 viral mRNA transcripts that encode two structural proteins (VP1 and VP2) and three nonstructural proteins (NS1, 7.5-kDa protein, and 11-kDa protein). Splicing at the second 5′ donor site (D2 site) of the B19V pre-mRNA is essential for the expression of VP2 and the 11-kDa protein. We previously identified thatcis-acting intronic splicing enhancer 2 (ISE2) that lies immediately after the D2 site facilitates the recognition of the D2

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Ameri, Afshin, Deepa K. Machiah, Darlene Livingston, et al. "A Novel 5bp Deletion Mutation in the Factor X (FX) Gene, Designated FX-Augusta, Causes Severe FX Deficiency Possibly by a Unique Mechanism Involving mRNAs that Lack Inframe Stop Codons." Blood 104, no. 11 (2004): 1045. http://dx.doi.org/10.1182/blood.v104.11.1045.1045.

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Abstract Due to its position in the coagulation cascade, factor X (fX), a circulating zymogen is activated during hemostatic challenges to its serine protease fXa first via the extrinsic pathway’s tissue factor/factor VIIa complex and next by the intrinsic Xase complex of factors Ixa and VIIIa on phospholipids membranes. Among the congenital factor abnormalities manifesting as hemorrhagic predispositions, fX deficiency states, which are often autosomal recessive and associated with consanguinity, are among the rarest. Since concurrent studies on the unrelated Stuart and Prower kindreds in the

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Hernandez, Victor A., Jessika Carvajal-Moreno, Xinyi Wang, Maciej Pietrzak, Jack C. Yalowich та Terry S. Elton. "Use of CRISPR/Cas9 with homology-directed repair to silence the human topoisomerase IIα intron-19 5’ splice site: Generation of etoposide resistance in human leukemia K562 cells". PLOS ONE 17, № 5 (2022): e0265794. http://dx.doi.org/10.1371/journal.pone.0265794.

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DNA Topoisomerase IIα (TOP2α/170) is an enzyme essential for proliferating cells. For rapidly multiplying malignancies, this has made TOP2α/170 an important target for etoposide and other clinically active anticancer drugs. Efficacy of these agents is often limited by chemoresistance related to alterations in TOP2α/170 expression levels. Our laboratory recently demonstrated reduced levels of TOP2α/170 and overexpression of a C-terminal truncated 90-kDa isoform, TOP2α/90, due to intronic polyadenylation (IPA; within intron 19) in an acquired etoposide-resistant K562 clonal cell line, K/VP.5. We

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Millar, R., D. Conklin, C. Lofton-Day, et al. "A novel human GnRH receptor homolog gene: abundant and wide tissue distribution of the antisense transcript." Journal of Endocrinology 162, no. 1 (1999): 117–26. http://dx.doi.org/10.1677/joe.0.1620117.

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Gonadotropin releasing hormone (GnRH) regulates the reproductive system through a specific G-protein-coupled receptor (GPCR) in pituitary gonadotropes. The existence of two (or more) forms of GnRH in most vertebrates suggested the existence of GnRH receptor subtypes (I and II). Using sequence information for extracellular loop 3 of a putative Type II GnRH receptor from a reptile species, we have looked for a Type II GnRH receptor gene in the human genome EST (expressed sequence tag) database. A homolog was identified which has 45% and 41% amino acid identity with exons 2 and 3 of the known hum

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Frank, Sander, Ilsa Coleman, Navonil De Sarkar, Dmytro Rudoy, Valeri Vasioukhin, and Pete Nelson. "Abstract B060: Characterization of DNA repair defects in CDK12 mutant prostate cancer and the identification of differential vulnerabilities." Cancer Research 83, no. 11_Supplement (2023): B060. http://dx.doi.org/10.1158/1538-7445.prca2023-b060.

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Abstract Background: CDK12 expression is lost in ~5% of metastatic castration-resistant prostate cancer (mCRPC) and associates with aggressive disease. Previous literature, based on acute CDK12-loss models, proposes a mechanism where CDK12 loss leads to a homologous recombination deficiency (HRD) phenotype via premature intronic polyadenylation of classic HR pathway genes, including BRCA1 and BRCA2. Cyclin K is an essential gene and functions in a heterodimer with CDK12 or CDK13. We sought to test if CDK12 loss: (1) confers HRD and a corresponding sensitivity to platinum and poly-ADP ribose po

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Cooke, Charles, and James C. Alwine. "Characterization of Specific Protein-RNA Complexes Associated with the Coupling of Polyadenylation and Last-Intron Removal." Molecular and Cellular Biology 22, no. 13 (2002): 4579–86. http://dx.doi.org/10.1128/mcb.22.13.4579-4586.2002.

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ABSTRACT Polyadenylation and splicing are highly coordinated on substrate RNAs capable of coupled polyadenylation and splicing. Individual elements of both splicing and polyadenylation signals are required for the in vitro coupling of the processing reactions. In order to understand more about the coupling mechanism, we examined specific protein-RNA complexes formed on RNA substrates, which undergo coupled splicing and polyadenylation. We hypothesized that formation of a coupling complex would be adversely affected by mutations of either splicing or polyadenylation elements known to be require

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Tian, B., Z. Pan, and J. Y. Lee. "Widespread mRNA polyadenylation events in introns indicate dynamic interplay between polyadenylation and splicing." Genome Research 17, no. 2 (2007): 156–65. http://dx.doi.org/10.1101/gr.5532707.

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