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Journal articles on the topic 'Genome wide screening'

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Published: 10 December 2022
Last updated: 10 March 2023

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1

Tsuchihara, Katsuya. "Nation-wide genome screening data-base." Annals of Oncology 28 (October 2017): ix19. http://dx.doi.org/10.1093/annonc/mdx551.

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2

Kamath, R. "Genome-wide RNAi screening in Caenorhabditis elegans." Methods 30, no. 4 (August 2003): 313–21. http://dx.doi.org/10.1016/s1046-2023(03)00050-1.

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3

LaFlamme, Brooke. "A CRISPR method for genome-wide screening." Nature Genetics 46, no. 2 (January 29, 2014): 99. http://dx.doi.org/10.1038/ng.2887.

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4

Livak, Kenneth J., Jeffrey Marmaro, and John A. Todd. "Towards fully automated genome–wide polymorphism screening." Nature Genetics 9, no. 4 (April 1995): 341–42. http://dx.doi.org/10.1038/ng0495-341.

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5

Han, Chan-Hee, In-Hwan Song, and Si-Woong Lee. "Automatic Segmentation of Cellular Images for High-Throughput Genome-Wide RNA Interference Screening." Journal of the Korea Contents Association 10, no. 4 (April 28, 2010): 19–27. http://dx.doi.org/10.5392/jkca.2010.10.4.019.

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6

Shaffer, Catherine. "CRISPR's Rapid Rise Shakes Up Genome-Wide Screening." Genetic Engineering & Biotechnology News 41, no. 5 (May 1, 2021): 46–49. http://dx.doi.org/10.1089/gen.41.05.13.

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7

Yu, Jason S. L., and Kosuke Yusa. "Genome-wide CRISPR-Cas9 screening in mammalian cells." Methods 164-165 (July 2019): 29–35. http://dx.doi.org/10.1016/j.ymeth.2019.04.015.

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8

Lee, C. Y. Daniel, and X. William Yang. "Huntington's Disease: Genome-wide Neuroprotection Screening Goes Viral." Neuron 106, no. 1 (April 2020): 4–6. http://dx.doi.org/10.1016/j.neuron.2020.03.020.

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9

Guseh, Stephanie, Louise Wilkins-Haug, Anjali J. Kaimal, Lisa Dunn Albanese, and Kathryn J. Gray. "81: Utility of non-invasive genome-wide screening." American Journal of Obstetrics and Gynecology 222, no. 1 (January 2020): S67—S68. http://dx.doi.org/10.1016/j.ajog.2019.11.097.

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10

García, Patricia, Javier Encinar del Dedo, José Ayté, and Elena Hidalgo. "Genome-wide Screening of Regulators of Catalase Expression." Journal of Biological Chemistry 291, no. 2 (November 13, 2015): 790–99. http://dx.doi.org/10.1074/jbc.m115.696658.

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11

Lee, Il-Kwon, Nan Young Kim, Hee Nam Kim, Dong Kyun Han, Hee-Jo Baek, Tai Ju Hwang, Hoon Kook, and Hyeoung Joon Kim. "Genome-Wide Screening of Copy Number Variation In Childhood Neuroblastoma." Blood 116, no. 21 (November 19, 2010): 4454. http://dx.doi.org/10.1182/blood.v116.21.4454.4454.

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Abstract Abstract 4454 Background Structural genetic variation, including copy-number variation (CNV), constitutes a substantial fraction of total genetic variability and the importance of structural variants in modulating human disease is increasingly being recognized. Recent studies showed that chromosomal aberrations are detectable in childhood cancers and can be associated with susceptibility to childhood cancers. However its relationship with neuroblosatoma in particular is not fully understood. To gain insight into the incidence of the chromosomal aberrations in neuroblastoma in children, we examined Korean childhood neuroblastoma genomes using high-resolution single-nucleotide polymorphism (SNP) array-based analysis. Patients and Methods 13 cases analyzed had been diagnosed with neuroblastoma (5 male, 8 female). 620,901 SNP markers were considered on these samples using Human610Quad v1.0 DNA analysis BeadChip (Illumina). Fragmented DNAs were hybridized on bead chips. Data analysis was carried out with GenomeStudio v2009.1, Genotyping 1.1.9, cnvPartition_v2.4.4 softwares. Overall call rate were more than 99.8%. Genome-wide CNV, genotyping of markers including 7,577 non-synonymous SNPs, loss of heterozygosity (LOH) analyses were performed using the GenomeStudio v2010.1. Linkage disequilibrium was analyzed by Haploview 4.2. The gene set enrichment analysis was performed using GO software, Panther. Results The average call rates were 99.8 %. In total 343 CNVs were identified across the whole genome. Average number of CNVs per genome in this study (17.15) is higher than that of CNVs called in the recent studies using lower-resolution SNP- or CNV arrays. The median size of CNVs was 30,056 (range 569 ~ 1,260,297 bp). The largest portion of CNVs (235 calls) were found to be 10 kb~500 kb in length. Gain/loss of CNV was 2.05/4.90 having 2.4 fold higher frequencies in loss calls. We defined CNV regions (CNVRs) by merging overlapping CNVs (30% of overlap threshold) detected in two or more genomes. In total 155 CNVRs identified. The median size of CNVR was 27,482 (range 806 ~ 1,270,815 bp). Like CNVs, CNVRs-losses were more frequent than CNVR-gains. Defined CNVRs encompassing 13.4Mb accounted for ~0.5% of the human genome. Total of 1029 NM numbered transcripts were located near or within the 155 CNVRs. Through gene ontology (GO) analysis, putative target genes within the commonly gained or deleted region were categorized. Gene functions significantly enriched in the identified CNVRs include receptors for signal transduction pathways, transcription factors with nucleic acid binding proteins, transporters and regulatory molecule related functions involved in developmental processes. Genotype distributions for 7,577 non-synonymous SNPs in neuroblastoma were also examined and compared to two lab-specific as well as 90 Korean HapMap samples as control reference. Conclusions High-resolution single-nucleotide polymorphism (SNP) array-based analysis allowed us a high incidence of gains and losses in childhood neuroblastoma. Many of those detectable legions were found to be previously unidentified cryptic chromosomal aberrations. Those CNVRs could be potentially Korean-specific novel CNVRs indicating that previous CNV coverage of the human genome is incomplete and there is human genome diversity among different ethnic populations. Although results reveals high degrees of heterogeneity in the genomic alterations detectable in neuroblastoma, genes of the signal transduction pathway and transcriptional regulatory members were the most frequently altered targets whose deregulation may play a role in the pathogenesis of neuroblastoma in children. CNVs/CNVRs identified in the study will be solid resources for investigating chromosomal aberrations in childhood cancer and its potential association with childhood neuroblastoma. Further studies on larger sample size, as well as functional analyses will define their role in the pathogenesis of neuroblastoma in children. Disclosures: No relevant conflicts of interest to declare.
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12

Veeneman, Brendan, Ying Gao, Joy Grant, David Fruhling, James Ahn, Benedikt Bosbach, Jadwiga Bienkowska, et al. "PINCER: improved CRISPR/Cas9 screening by efficient cleavage at conserved residues." Nucleic Acids Research 48, no. 17 (August 21, 2020): 9462–77. http://dx.doi.org/10.1093/nar/gkaa645.

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Abstract CRISPR/Cas9 functional genomic screens have emerged as essential tools in drug target discovery. However, the sensitivity of available genome-wide CRISPR libraries is impaired by guides which inefficiently abrogate gene function. While Cas9 cleavage efficiency optimization and essential domain targeting have been developed as independent guide design rationales, no library has yet combined these into a single cohesive strategy to knock out gene function. Here, in a massive reanalysis of CRISPR tiling data using the most comprehensive feature database assembled, we determine which features of guides and their targets best predict activity and how to best combine them into a single guide design algorithm. We present the ProteIN ConsERvation (PINCER) genome-wide CRISPR library, which for the first time combines enzymatic efficiency optimization with conserved length protein region targeting, and also incorporates domains, coding sequence position, U6 termination (TTT), restriction sites, polymorphisms and specificity. Finally, we demonstrate superior performance of the PINCER library compared to alternative genome-wide CRISPR libraries in head-to-head validation. PINCER is available for individual gene knockout and genome-wide screening for both the human and mouse genomes.
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13

Jaaro, Hanna, Zehava Levy, and Mike Fainzilber. "A Genome Wide Screening Approach for Membrane-targeted Proteins." Molecular & Cellular Proteomics 4, no. 3 (December 31, 2004): 328–33. http://dx.doi.org/10.1074/mcp.t400020-mcp200.

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14

Sanjana, Neville E., Ophir Shalem, and Feng Zhang. "Improved vectors and genome-wide libraries for CRISPR screening." Nature Methods 11, no. 8 (July 30, 2014): 783–84. http://dx.doi.org/10.1038/nmeth.3047.

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15

Roses, Allen D. "Genome-wide screening for drug discovery and companion diagnostics." Expert Opinion on Drug Discovery 2, no. 4 (April 2007): 489–501. http://dx.doi.org/10.1517/17460441.2.4.489.

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16

Rong, Yao, Shota Nakamura, Tetsuya Hirata, Daisuke Motooka, Yi-Shi Liu, Zeng-An He, Xiao-Dong Gao, Yusuke Maeda, Taroh Kinoshita, and Morihisa Fujita. "Genome-Wide Screening of Genes Required for Glycosylphosphatidylinositol Biosynthesis." PLOS ONE 10, no. 9 (September 18, 2015): e0138553. http://dx.doi.org/10.1371/journal.pone.0138553.

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17

Singh, Arunima. "Genome-wide high-throughput screening of T cell epitopes." Nature Methods 16, no. 10 (September 27, 2019): 953. http://dx.doi.org/10.1038/s41592-019-0599-0.

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18

Schroeder, Christopher, Arif Bülent Ekici, Ute Moog, Ute Grasshoff, Ulrike Mau-Holzmann, Marc Sturm, Vanessa Vosseler, et al. "Genome-wide UPD screening in patients with intellectual disability." European Journal of Human Genetics 22, no. 10 (May 7, 2014): 1233–35. http://dx.doi.org/10.1038/ejhg.2014.63.

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19

Sidik, Saima M., Diego Huet, and Sebastian Lourido. "CRISPR-Cas9-based genome-wide screening of Toxoplasma gondii." Nature Protocols 13, no. 2 (January 11, 2018): 307–23. http://dx.doi.org/10.1038/nprot.2017.131.

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20

Kakimoto, Masayuki, Atsushi Kobayashi, Ryouichi Fukuda, Yasuke Ono, Akinori Ohta, and Etsuro Yoshimura. "Genome-Wide Screening of Aluminum Tolerance in Saccharomyces cerevisiae." BioMetals 18, no. 5 (October 2005): 467–74. http://dx.doi.org/10.1007/s10534-005-4663-0.

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21

Schnabel, Renate B. "Genome-Wide Genetic Association Study Meets Systematic Metabolite Screening." Circulation: Cardiovascular Genetics 5, no. 4 (August 2012): 479–80. http://dx.doi.org/10.1161/circgenetics.112.964239.

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22

Xu, Chunlong, Xiaolan Qi, Xuguang Du, Huiying Zou, Fei Gao, Tao Feng, Hengxing Lu, et al. "piggyBac mediates efficient in vivo CRISPR library screening for tumorigenesis in mice." Proceedings of the National Academy of Sciences 114, no. 4 (January 6, 2017): 722–27. http://dx.doi.org/10.1073/pnas.1615735114.

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CRISPR/Cas9 is becoming an increasingly important tool to functionally annotate genomes. However, because genome-wide CRISPR libraries are mostly constructed in lentiviral vectors, in vivo applications are severely limited as a result of difficulties in delivery. Here, we examined the piggyBac (PB) transposon as an alternative vehicle to deliver a guide RNA (gRNA) library for in vivo screening. Although tumor induction has previously been achieved in mice by targeting cancer genes with the CRISPR/Cas9 system, in vivo genome-scale screening has not been reported. With our PB-CRISPR libraries, we conducted an in vivo genome-wide screen in mice and identified genes mediating liver tumorigenesis, including known and unknown tumor suppressor genes (TSGs). Our results demonstrate that PB can be a simple and nonviral choice for efficient in vivo delivery of CRISPR libraries.
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23

Park, Eun-Hee, and Myoung-Dong Kim. "Genome-Wide Screening of Saccharomyces cerevisiae Genes Regulated by Vanillin." Journal of Microbiology and Biotechnology 25, no. 1 (January 28, 2015): 50–56. http://dx.doi.org/10.4014/jmb.1409.09064.

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24

KHAMAS, AHMED, TOSHIAKI ISHIKAWA, KAORU MOGUSHI, SATORU IIDA, MEGUMI ISHIGURO, HIROSHI TANAKA, HIROYUKI UETAKE, and KENICHI SUGIHARA. "Genome-wide screening for methylation-silenced genes in colorectal cancer." International Journal of Oncology 41, no. 2 (May 30, 2012): 490–96. http://dx.doi.org/10.3892/ijo.2012.1500.

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25

Mimura, Kaito, Jun-Ichi Sakamaki, Hideaki Morishita, Masahito Kawazu, Hiroyuki Mano, and Noboru Mizushima. "Genome-wide CRISPR screening reveals nucleotide synthesis negatively regulates autophagy." Journal of Biological Chemistry 296 (January 2021): 100780. http://dx.doi.org/10.1016/j.jbc.2021.100780.

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26

Gill, R. T., S. Wildt, Y. T. Yang, S. Ziesman, and G. Stephanopoulos. "Genome-wide screening for trait conferring genes using DNA microarrays." Proceedings of the National Academy of Sciences 99, no. 10 (May 7, 2002): 7033–38. http://dx.doi.org/10.1073/pnas.102154799.

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27

Popa, Stephanie, Julien Villeneuve, Sarah Stewart, Esther Perez Garcia, Anna Petrunkina Harrison, and Kevin Moreau. "Genome-wide CRISPR screening identifies new regulators of glycoprotein secretion." Wellcome Open Research 4 (August 9, 2019): 119. http://dx.doi.org/10.12688/wellcomeopenres.15232.1.

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Background: The fundamental process of protein secretion from eukaryotic cells has been well described for many years, yet gaps in our understanding of how this process is regulated remain. Methods: With the aim of identifying novel genes involved in the secretion of glycoproteins, we used a screening pipeline consisting of a pooled genome-wide CRISPR screen, followed by secondary siRNA screening of the hits to identify and validate several novel regulators of protein secretion. Results: We present approximately 50 novel genes not previously associated with protein secretion, many of which also had an effect on the structure of the Golgi apparatus. We further studied a small selection of hits to investigate their subcellular localisation. One of these, GPR161, is a novel Golgi-resident protein that we propose maintains Golgi structure via an interaction with golgin A5. Conclusions: This study has identified new factors for protein secretion involved in Golgi homeostasis.
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28

Popa, Stephanie, Julien Villeneuve, Sarah Stewart, Esther Perez Garcia, Anna Petrunkina Harrison, and Kevin Moreau. "Genome-wide CRISPR screening identifies new regulators of glycoprotein secretion." Wellcome Open Research 4 (January 16, 2020): 119. http://dx.doi.org/10.12688/wellcomeopenres.15232.2.

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Background: The fundamental process of protein secretion from eukaryotic cells has been well described for many years, yet gaps in our understanding of how this process is regulated remain. Methods: With the aim of identifying novel genes involved in the secretion of glycoproteins, we used a screening pipeline consisting of a pooled genome-wide CRISPR screen, followed by secondary siRNA screening of the hits to identify and validate several novel regulators of protein secretion. Results: We present approximately 50 novel genes not previously associated with protein secretion, many of which also had an effect on the structure of the Golgi apparatus. We further studied a small selection of hits to investigate their subcellular localisation. One of these, GPR161, is a novel Golgi-resident protein that we propose maintains Golgi structure via an interaction with golgin A5. Conclusions: This study has identified new factors for protein secretion involved in Golgi homeostasis.
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29

Medico, Enzo, Alessandra Gentile, Philippe Soriano, and Paolo Comoglio. "A genome-wide trap screening procedure for transcriptionally responsive genes." Nature Genetics 27, S4 (April 2001): 73. http://dx.doi.org/10.1038/87208.

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30

Lobingier, Braden, Nikoleta Tsvetanova, and Mark von Zastrow. "Chemical Biology Approaches for Genome‐Wide Screening of GPCR Trafficking." FASEB Journal 34, S1 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.05794.

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31

Liu, Yaowu, and Jun Xie. "Powerful test based on conditional effects for genome-wide screening." Annals of Applied Statistics 12, no. 1 (March 2018): 567–85. http://dx.doi.org/10.1214/17-aoas1103.

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32

Urh, Kristian, and Tanja Kunej. "Genome-wide screening for smallest regions of overlaps in cryptorchidism." Reproductive BioMedicine Online 37, no. 1 (July 2018): 85–99. http://dx.doi.org/10.1016/j.rbmo.2018.02.008.

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33

Mair, Barbara, Peter M. Aldridge, Randy S. Atwal, David Philpott, Meng Zhang, Sanna N. Masud, Mahmoud Labib, et al. "High-throughput genome-wide phenotypic screening via immunomagnetic cell sorting." Nature Biomedical Engineering 3, no. 10 (September 23, 2019): 796–805. http://dx.doi.org/10.1038/s41551-019-0454-8.

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34

Fiorentino, Francesco, Sara Bono, Francesca Pizzuti, Sara Duca, Arianna Polverari, Monica Faieta, Marina Baldi, Laura Diano, and Francesca Spinella. "The clinical utility of genome-wide non invasive prenatal screening." Prenatal Diagnosis 37, no. 6 (May 12, 2017): 593–601. http://dx.doi.org/10.1002/pd.5053.

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35

Lemos, Samara M. C., Luiz F. C. Fonçatti, Romain Guyot, Alexandre R. Paschoal, and Douglas S. Domingues. "Genome-Wide Screening and Characterization of Non-Coding RNAs in Coffea canephora." Non-Coding RNA 6, no. 3 (September 11, 2020): 39. http://dx.doi.org/10.3390/ncrna6030039.

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Coffea canephora grains are highly traded commodities worldwide. Non-coding RNAs (ncRNAs) are transcriptional products involved in genome regulation, environmental responses, and plant development. There is not an extensive genome-wide analysis that uncovers the ncRNA portion of the C. canephora genome. This study aimed to provide a curated characterization of six ncRNA classes in the Coffea canephora genome. For this purpose, we employed a combination of similarity-based and structural-based computational approaches with stringent curation. Candidate ncRNA loci had expression evidence analyzed using sRNA-seq libraries. We identified 7455 ncRNA loci (6976 with transcriptional evidence) in the C. canephora genome. This comprised of total 115 snRNAs, 1031 snoRNAs, 92 miRNA precursors, 602 tRNAs, 72 rRNAs, and 5064 lncRNAs. For miRNAs, we identified 159 putative high-confidence targets. This study was the most extensive genomic catalog of curated ncRNAs in the Coffea genus. This data might help elaborating more robust hypotheses in future comparative genomic studies as well as gene regulation and genome dynamics, helping to understand the molecular basis of domestication, environmental adaptation, resistance to pests and diseases, and coffee productivity.
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36

Wang, Xiaoyi, Yanping Han, Yanjun Li, Zhaobiao Guo, Yajun Song, Yafang Tan, Zongmin Du, Alexander Rakin, Dongsheng Zhou, and Ruifu Yang. "Yersinia genome diversity disclosed by Yersinia pestis genome-wide DNA microarray." Canadian Journal of Microbiology 53, no. 11 (November 2007): 1211–21. http://dx.doi.org/10.1139/w07-087.

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The genus Yersinia includes 11 species, 3 of which ( Y. pestis , Y. pseudotuberculosis , and Y. enterocolitica ) are pathogenic for humans. The remaining 8 species ( Y. frederiksenii , Y. intermedia , Y. kristensenii , Y. bercovieri , Y. mollaretii , Y. rohdei , Y. ruckeri , and Y. aldovae ) are merely opportunistic pathogens found mostly in the environment. In this work, the genomic differences among Yersinia were determined using a Y. pestis-specific DNA microarray. The results revealed 292 chromosomal genes that were shared by all Yersinia species tested, constituting the conserved gene pool of the genus Yersinia. Hierarchical clustering analysis of the microarray data revealed the genetic relationships among all 11 species in this genus. The microarray analysis in conjunction with PCR screening greatly reduced the number of chromosomal genes (32) specific for Y. pestis to 16 genes and uncovered a high level of genomic plasticity within Y. pseudotuberculosis, indicating that its different serotypes have undergone an extensively parallel loss or acquisition of genetic content, which is likely to be important for its adaptation to changes in environmental niches.
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37

Chen, Hao, Jessica Wilson, Carson Ercanbrack, Hannah Smith, Qinglei Gan, and Chenguang Fan. "Genome-Wide Screening of Oxidizing Agent Resistance Genes in Escherichia coli." Antioxidants 10, no. 6 (May 27, 2021): 861. http://dx.doi.org/10.3390/antiox10060861.

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The use of oxidizing agents is one of the most favorable approaches to kill bacteria in daily life. However, bacteria have been evolving to survive in the presence of different oxidizing agents. In this study, we aimed to obtain a comprehensive list of genes whose expression can make Escherichiacoli cells resistant to different oxidizing agents. For this purpose, we utilized the ASKA library and performed a genome-wide screening of ~4200 E. coli genes. Hydrogen peroxide (H2O2) and hypochlorite (HOCl) were tested as representative oxidizing agents in this study. To further validate our screening results, we used different E. coli strains as host cells to express or inactivate selected resistance genes individually. More than 100 genes obtained in this screening were not known to associate with oxidative stress responses before. Thus, this study is expected to facilitate both basic studies on oxidative stress and the development of antibacterial agents.
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38

Yin, Zixi, and Lingyi Chen. "Simple Meets Single: The Application of CRISPR/Cas9 in Haploid Embryonic Stem Cells." Stem Cells International 2017 (2017): 1–6. http://dx.doi.org/10.1155/2017/2601746.

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The CRISPR/Cas9 system provides a powerful method for the genetic manipulation of the mammalian genome, allowing knockout of individual genes as well as the generation of genome-wide knockout cell libraries for genetic screening. However, the diploid status of most mammalian cells restricts the application of CRISPR/Cas9 in genetic screening. Mammalian haploid embryonic stem cells (haESCs) have only one set of chromosomes per cell, avoiding the issue of heterozygous recessive mutations in diploid cells. Thus, the combination of haESCs and CRISPR/Cas9 facilitates the generation of genome-wide knockout cell libraries for genetic screening. Here, we review recent progress in CRISPR/Cas9 and haPSCs and discuss their applications in genetic screening.
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39

Kampmann, Martin, Max A. Horlbeck, Yuwen Chen, Jordan C. Tsai, Michael C. Bassik, Luke A. Gilbert, Jacqueline E. Villalta, et al. "Next-generation libraries for robust RNA interference-based genome-wide screens." Proceedings of the National Academy of Sciences 112, no. 26 (June 15, 2015): E3384—E3391. http://dx.doi.org/10.1073/pnas.1508821112.

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Genetic screening based on loss-of-function phenotypes is a powerful discovery tool in biology. Although the recent development of clustered regularly interspaced short palindromic repeats (CRISPR)-based screening approaches in mammalian cell culture has enormous potential, RNA interference (RNAi)-based screening remains the method of choice in several biological contexts. We previously demonstrated that ultracomplex pooled short-hairpin RNA (shRNA) libraries can largely overcome the problem of RNAi off-target effects in genome-wide screens. Here, we systematically optimize several aspects of our shRNA library, including the promoter and microRNA context for shRNA expression, selection of guide strands, and features relevant for postscreen sample preparation for deep sequencing. We present next-generation high-complexity libraries targeting human and mouse protein-coding genes, which we grouped into 12 sublibraries based on biological function. A pilot screen suggests that our next-generation RNAi library performs comparably to current CRISPR interference (CRISPRi)-based approaches and can yield complementary results with high sensitivity and high specificity.
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40

Mohammadi, Elyas, Rui Benfeitas, Hasan Turkez, Jan Boren, Jens Nielsen, Mathias Uhlen, and Adil Mardinoglu. "Applications of Genome-Wide Screening and Systems Biology Approaches in Drug Repositioning." Cancers 12, no. 9 (September 21, 2020): 2694. http://dx.doi.org/10.3390/cancers12092694.

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Modern drug discovery through de novo drug discovery entails high financial costs, low success rates, and lengthy trial periods. Drug repositioning presents a suitable approach for overcoming these issues by re-evaluating biological targets and modes of action of approved drugs. Coupling high-throughput technologies with genome-wide essentiality screens, network analysis, genome-scale metabolic modeling, and machine learning techniques enables the proposal of new drug–target signatures and uncovers unanticipated modes of action for available drugs. Here, we discuss the current issues associated with drug repositioning in light of curated high-throughput multi-omic databases, genome-wide screening technologies, and their application in systems biology/medicine approaches.
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41

Yahagi, Naoya, and Yoshinori Takeuchi. "Genome-wide screening of upstream transcription factors using an expression library." F1000Research 10 (January 28, 2021): 51. http://dx.doi.org/10.12688/f1000research.27532.1.

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The identification of upstream transcription factors regulating the expression of a gene is generally not an easy process. To facilitate this task, we constructed an expression cDNA library named Transcription Factor Expression Library (TFEL), which is composed of nearly all the transcription factors in the mouse genome. Genome-wide screening using this library (TFEL scan method) enables us to easily identify transcription factors controlling any given promoter or enhancer of interest in a chromosomal context-dependent manner. Thus, TFEL scan method is a powerful approach to explore transcriptional regulatory networks.
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42

Yahagi, Naoya, and Yoshinori Takeuchi. "Genome-wide screening of upstream transcription factors using an expression library." F1000Research 10 (March 8, 2021): 51. http://dx.doi.org/10.12688/f1000research.27532.2.

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The identification of upstream transcription factors regulating the expression of a gene is generally not an easy process. To facilitate this task, we constructed an expression cDNA library named Transcription Factor Expression Library (TFEL), which is composed of nearly all the transcription factors in the mouse genome. Genome-wide screening using this library (TFEL scan method) enables us to easily identify transcription factors controlling any given promoter or enhancer of interest in a chromosomal context-dependent manner. Thus, TFEL scan method is a powerful approach to explore transcriptional regulatory networks.
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43

Ribeiro Reily Rocha, Clarissa, Alexandre Reily Rocha, Matheus Molina Silva, Luciana Rodrigues Gomes, Marcela Teatin Latancia, Marina Andrade Tomaz, Izadora de Souza, Linda Karolynne Seregni Monteiro, and Carlos Frederico Martins Menck. "Revealing Temozolomide Resistance Mechanisms via Genome-Wide CRISPR Libraries." Cells 9, no. 12 (December 1, 2020): 2573. http://dx.doi.org/10.3390/cells9122573.

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Glioblastoma is a severe type of brain tumor with a poor prognosis and few therapy options. Temozolomide (TMZ) is one of these options, however, with limited success, and failure is mainly due to tumor resistance. In this work, genome-wide CRISPR-Cas9 lentiviral screen libraries for gene knockout or activation were transduced in the human glioblastoma cell line, aiming to identify genes that modulate TMZ resistance. The sgRNAs enriched in both libraries in surviving cells after TMZ treatment were identified by next-generation sequencing (NGS). Pathway analyses of gene candidates on knockout screening revealed several enriched pathways, including the mismatch repair and the Sonic Hedgehog pathways. Silencing three genes ranked on the top 10 list (MSH2, PTCH2, and CLCA2) confirm cell protection from TMZ-induced death. In addition, a CRISPR activation library revealed that NRF2 and Wnt pathways are involved in TMZ resistance. Consistently, overexpression of FZD6, CTNNB1, or NRF2 genes significantly increased cell survival upon TMZ treatment. Moreover, NRF2 and related genes detected in this screen presented a robust negative correlation with glioblastoma patient survival rates. Finally, several gene candidates from knockout or activation screening are targetable by inhibitors or small molecules, and some of them have already been used in the clinic.
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Chang, Hao, Yukun Pan, Sean Landrette, Sheng Ding, Dong Yang, Lufang Liu, Lei Tian, et al. "Efficient genome-wide first-generation phenotypic screening system in mice using thepiggyBactransposon." Proceedings of the National Academy of Sciences 116, no. 37 (August 26, 2019): 18507–16. http://dx.doi.org/10.1073/pnas.1906354116.

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Genome-wide phenotypic screens provide an unbiased way to identify genes involved in particular biological traits, and have been widely used in lower model organisms. However, cost and time have limited the utility of such screens to address biological and disease questions in mammals. Here we report a highly efficientpiggyBac(PB) transposon-based first-generation (F1) dominant screening system in mice that enables an individual investigator to conduct a genome-wide phenotypic screen within a year with fewer than 300 cages. ThePBscreening system uses visually trackable transposons to induce both gain- and loss-of-function mutations and generates genome-wide distributed new insertions in more than 55% of F1 progeny. Using this system, we successfully conducted a pilot F1 screen and identified 5 growth retardation mutations. One of these mutants, a Six1/4PB/+mutant, revealed a role in milk intake behavior. The mutant animals exhibit abnormalities in nipple recognition and milk ingestion, as well as developmental defects in cranial nerves V, IX, and X. ThisPBF1 screening system offers individual laboratories unprecedented opportunities to conduct affordable genome-wide phenotypic screens for deciphering the genetic basis of mammalian biology and disease pathogenesis.
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Feng, Yujie, Xiao Hu, Kai Ma, Bingyuan Zhang, and Chuandong Sun. "Genome-Wide Screening Identifies Prognostic Long Noncoding RNAs in Hepatocellular Carcinoma." BioMed Research International 2021 (May 20, 2021): 1–16. http://dx.doi.org/10.1155/2021/6640652.

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Hepatocellular carcinoma (HCC) is a common malignancy with a poor prognosis. Therefore, there is an urgent call for the investigation of novel biomarkers in HCC. In the present study, we identified 6 upregulated lncRNAs in HCC, including LINC01134, RHPN1-AS1, NRAV, CMB9-22P13.1, MKLN1-AS, and MAPKAPK5-AS1. Higher expression of these lncRNAs was correlated to a more advanced cancer stage and a poorer prognosis in HCC patients. Enrichment analysis revealed that these lncRNAs played a crucial role in HCC progression, possibly through a series of cancer-related biological processes, such as cell cycle, DNA replication, histone acetyltransferase complex, fatty acid oxidation, and lipid modification. Moreover, competing endogenous RNA (ceRNA) network analysis revealed that these lncRNAs could bind to certain miRNAs to promote HCC progression. Loss-of-function assays indicated that silencing of RHPN1-AS1 significantly suppressed HCC proliferation and migration. Though further validations are still needed, these identified lncRNAs could serve as valuable potential biomarkers for HCC prognosis.
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Xu, Xiao-Yan, Xiao-Wei Wei, Wei Ma, Hui Gu, Dan Liu, and Zheng-Wei Yuan. "Genome-Wide Screening of Aberrant Methylation Loci for Nonsyndromic Cleft Lip." Chinese Medical Journal 131, no. 17 (September 2018): 2055–62. http://dx.doi.org/10.4103/0366-6999.239305.

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Jarjanazi, Hamdi, Hong Li, Irene L. Andrulis, and Hilmi Ozcelik. "Genome Wide Screening of CAG Trinucleotide Repeat Lengths in Breast Cancer." Disease Markers 22, no. 5-6 (2006): 343–49. http://dx.doi.org/10.1155/2006/951857.

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Trinucleotide repeat sequences are widely present in the human genome. The expansion of CAG repeats have been studied very extensively, and shown to be the causative mechanism of more than 40 neuromuscular and neurodegenerative diseases. In the present study, we performed a genome wide screening of CAG repeat expansions in non-neoplastic tissues of 212 breast cancer cases and 196 healthy population controls using the Repeat Expansion Detection (RED) method. Distribution of CAG repeat lengths in cases was not significantly different from controls. However, dramatically expanded CAG repeats were detected in 2.4% (n= 5) of breast cancer cases where no repeats of similar size were detected in any of the healthy population controls. Although this trend shows only borderline significance (p= 0.06), this finding suggests a potential involvement of CAG repeat expansion in breast cancer susceptibility. These repeats may potentially affect the function of cancer predisposition genes, with a similar mechanism as in neurodegenerative and neuromuscular disorders.
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Forment, Josep V., Mareike Herzog, Julia Coates, Tomasz Konopka, Bianca V. Gapp, Sebastian M. Nijman, David J. Adams, Thomas M. Keane, and Stephen P. Jackson. "Genome-wide genetic screening with chemically mutagenized haploid embryonic stem cells." Nature Chemical Biology 13, no. 1 (October 31, 2016): 12–14. http://dx.doi.org/10.1038/nchembio.2226.

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Cullen, Lara M., and Greg M. Arndt. "Genome‐wide screening for gene function using RNAi in mammalian cells." Immunology & Cell Biology 83, no. 3 (June 2005): 217–23. http://dx.doi.org/10.1111/j.1440-1711.2005.01332.x.

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Singh, Arunima. "Author Correction: Genome-wide high-throughput screening of T cell epitopes." Nature Methods 16, no. 12 (October 29, 2019): 1332. http://dx.doi.org/10.1038/s41592-019-0660-z.

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