Artykuły w czasopismach na temat „GGGGCC repeats”
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Jiao, Bin, Mengli Wang, Hao Feng, Han Bao, Feiran Zhang, Hao Wu, Junling Wang, Beisha Tang, Peng Jin i Lu Shen. "Downregulation of TOP2 modulates neurodegeneration caused by GGGGCC expanded repeats". Human Molecular Genetics 30, nr 10 (22.03.2021): 893–901. http://dx.doi.org/10.1093/hmg/ddab079.
Pełny tekst źródłaLiu, Xiaole, Xinyue Zhao, Jinhan He, Sishi Wang, Xinfei Shen, Qingfeng Liu i Shenlin Wang. "Advances in the Structure of GGGGCC Repeat RNA Sequence and Its Interaction with Small Molecules and Protein Partners". Molecules 28, nr 15 (1.08.2023): 5801. http://dx.doi.org/10.3390/molecules28155801.
Pełny tekst źródłavan ‘t Spijker, Heleen M., Emily E. Stackpole, Sandra Almeida, Olga Katsara, Botao Liu, Kuang Shen, Robert J. Schneider, Fen-Biao Gao i Joel D. Richter. "Ribosome profiling reveals novel regulation of C9ORF72 GGGGCC repeat-containing RNA translation". RNA 28, nr 2 (30.11.2021): 123–38. http://dx.doi.org/10.1261/rna.078963.121.
Pełny tekst źródłaBabić Leko, Mirjana, Vera Župunski, Jason Kirincich, Dinko Smilović, Tibor Hortobágyi, Patrick R. Hof i Goran Šimić. "Molecular Mechanisms of Neurodegeneration Related to C9orf72 Hexanucleotide Repeat Expansion". Behavioural Neurology 2019 (15.01.2019): 1–18. http://dx.doi.org/10.1155/2019/2909168.
Pełny tekst źródłaHatanaka, Yukari, Tomohiro Umeda, Keiko Shigemori, Toshihide Takeuchi, Yoshitaka Nagai i Takami Tomiyama. "C9orf72 Hexanucleotide Repeat Expansion-Related Neuropathology Is Attenuated by Nasal Rifampicin in Mice". Biomedicines 10, nr 5 (6.05.2022): 1080. http://dx.doi.org/10.3390/biomedicines10051080.
Pełny tekst źródłaZhang, Yong-Jie, Lin Guo, Patrick K. Gonzales, Tania F. Gendron, Yanwei Wu, Karen Jansen-West, Aliesha D. O’Raw i in. "Heterochromatin anomalies and double-stranded RNA accumulation underlie C9orf72 poly(PR) toxicity". Science 363, nr 6428 (14.02.2019): eaav2606. http://dx.doi.org/10.1126/science.aav2606.
Pełny tekst źródłaHaeusler, Aaron R. "Nucleotide Structural Polymorphisms Formed by GGGGCC Repeats Cause C9orf72 Abortive Transcription and Nucleolar Stress". Biophysical Journal 106, nr 2 (styczeń 2014): 488a. http://dx.doi.org/10.1016/j.bpj.2013.11.4477.
Pełny tekst źródłaTeng, Ye, Ming Zhu i Zhidong Qiu. "G-quadruplexes in Repeat Expansion Disorders". International Journal of Molecular Sciences 24, nr 3 (25.01.2023): 2375. http://dx.doi.org/10.3390/ijms24032375.
Pełny tekst źródłaBalendra, Rubika, Igor Ruiz de los Mozos, Hana M. Odeh, Idoia Glaria, Carmelo Milioto, Katherine M. Wilson, Agnieszka M. Ule i in. "Transcriptome-wide RNA binding analysis of C9orf72 poly(PR) dipeptides". Life Science Alliance 6, nr 9 (12.07.2023): e202201824. http://dx.doi.org/10.26508/lsa.202201824.
Pełny tekst źródłaReddy, Kaalak, Monika H. M. Schmidt, Jaimie M. Geist, Neha P. Thakkar, Gagan B. Panigrahi, Yuh-Hwa Wang i Christopher E. Pearson. "Processing of double-R-loops in (CAG)·(CTG) and C9orf72 (GGGGCC)·(GGCCCC) repeats causes instability". Nucleic Acids Research 42, nr 16 (21.08.2014): 10473–87. http://dx.doi.org/10.1093/nar/gku658.
Pełny tekst źródłaTaki, Motahareh, Kushal J. Rohilla, Maria Barton, Madison Funneman, Najiyah Benzabeh, Swati Naphade, Lisa M. Ellerby, Keith T. Gagnon i Mohtashim H. Shamsi. "Novel probes for label-free detection of neurodegenerative GGGGCC repeats associated with amyotrophic lateral sclerosis". Analytical and Bioanalytical Chemistry 411, nr 26 (21.08.2019): 6995–7003. http://dx.doi.org/10.1007/s00216-019-02075-8.
Pełny tekst źródłaHalim, Dilara O., Gopinath Krishnan, Evan P. Hass, Soojin Lee, Mamta Verma, Sandra Almeida, Yuanzheng Gu, Deborah Y. Kwon, Thomas G. Fazzio i Fen-Biao Gao. "The exocyst subunit EXOC2 regulates the toxicity of expanded GGGGCC repeats in C9ORF72-ALS/FTD". Cell Reports 43, nr 7 (lipiec 2024): 114375. http://dx.doi.org/10.1016/j.celrep.2024.114375.
Pełny tekst źródłaDeJesus-Hernandez, Mariely, Ross A. Aleff, Jazmyne L. Jackson, NiCole A. Finch, Matthew C. Baker, Tania F. Gendron, Melissa E. Murray i in. "Long-read targeted sequencing uncovers clinicopathological associations for C9orf72-linked diseases". Brain 144, nr 4 (1.04.2021): 1082–88. http://dx.doi.org/10.1093/brain/awab006.
Pełny tekst źródłavan der Ende, Emma L., Jazmyne L. Jackson, Adrianna White, Harro Seelaar, Marka van Blitterswijk i John C. Van Swieten. "Unravelling the clinical spectrum and the role of repeat length in C9ORF72 repeat expansions". Journal of Neurology, Neurosurgery & Psychiatry 92, nr 5 (15.01.2021): 502–9. http://dx.doi.org/10.1136/jnnp-2020-325377.
Pełny tekst źródłaSatoh, Jun-Ichi, Yoji Yamamoto, Shouta Kitano, Mika Takitani, Naohiro Asahina i Yoshihiro Kino. "Molecular Network Analysis Suggests a Logical Hypothesis for the Pathological Role of C9orf72 in Amyotrophic Lateral Sclerosis/Frontotemporal Dementia". Journal of Central Nervous System Disease 6 (styczeń 2014): JCNSD.S18103. http://dx.doi.org/10.4137/jcnsd.s18103.
Pełny tekst źródłaCooper-Knock, Johnathan, Joanna J. Bury, Paul R. Heath, Matthew Wyles, Adrian Higginbottom, Catherine Gelsthorpe, J. Robin Highley i in. "C9ORF72 GGGGCC Expanded Repeats Produce Splicing Dysregulation which Correlates with Disease Severity in Amyotrophic Lateral Sclerosis". PLOS ONE 10, nr 5 (27.05.2015): e0127376. http://dx.doi.org/10.1371/journal.pone.0127376.
Pełny tekst źródłaShpilyukova, Yu A., E. Yu Fedotova, T. V. Pogoda, N. Yu Abramycheva, A. S. Vetchinova, M. N. Zakharova i S. N. Illarioshkin. "Evaluation of methylation status of the 5’-promoter region of C9orf72 gene in Russian patients with neurodegenerative diseases". Neuromuscular Diseases 8, nr 2 (20.07.2018): 33–41. http://dx.doi.org/10.17650/2222-8721-2018-8-2-33-41.
Pełny tekst źródłaOrmandzhiev, S., T. Todorov, T. Angelov, T. Chamova, V. Mitev, A. Todorova i I. Tournev. "Targeted Screening of the C9orf72 Gene in Bulgarian Amyotrophic Lateral Sclerosis Patients". Acta Medica Bulgarica 49, nr 1 (1.04.2022): 12–16. http://dx.doi.org/10.2478/amb-2022-0002.
Pełny tekst źródłaShi, Kevin Y., Eiichiro Mori, Zehra F. Nizami, Yi Lin, Masato Kato, Siheng Xiang, Leeju C. Wu i in. "Toxic PRn poly-dipeptides encoded by the C9orf72 repeat expansion block nuclear import and export". Proceedings of the National Academy of Sciences 114, nr 7 (9.01.2017): E1111—E1117. http://dx.doi.org/10.1073/pnas.1620293114.
Pełny tekst źródłaZhang, Yuan, Christopher Roland i Celeste Sagui. "Structural and Dynamical Characterization of DNA and RNA Quadruplexes Obtained from the GGGGCC and GGGCCT Hexanucleotide Repeats Associated with C9FTD/ALS and SCA36 Diseases". ACS Chemical Neuroscience 9, nr 5 (27.12.2017): 1104–17. http://dx.doi.org/10.1021/acschemneuro.7b00476.
Pełny tekst źródłaKaur, Jaslovleen, Shaista Parveen, Uzma Shamim, Pooja Sharma, Varun Suroliya, Akhilesh Kumar Sonkar, Istaq Ahmad i in. "Investigations of Huntington’s Disease and Huntington’s Disease-Like Syndromes in Indian Choreatic Patients". Journal of Huntington's Disease 9, nr 3 (8.10.2020): 283–89. http://dx.doi.org/10.3233/jhd-200398.
Pełny tekst źródłaHu, Jiaxin, Jing Liu, Liande Li, Keith T. Gagnon i David R. Corey. "Engineering Duplex RNAs for Challenging Targets: Recognition of GGGGCC/CCCCGG Repeats at the ALS/FTD C9orf72 Locus". Chemistry & Biology 22, nr 11 (listopad 2015): 1505–11. http://dx.doi.org/10.1016/j.chembiol.2015.09.016.
Pełny tekst źródłaKitano, Shouta, Yoshihiro Kino, Yoji Yamamoto, Mika Takitani, Junko Miyoshi, Tsuyoshi Ishida, Yuko Saito, Kunimasa Arima i Jun-Ichi Satoh. "Bioinformatics Data Mining Approach Suggests Coexpression of AGTPBP1 with an ALS-linked Gene C9orf72". Journal of Central Nervous System Disease 7 (styczeń 2015): JCNSD.S24317. http://dx.doi.org/10.4137/jcnsd.s24317.
Pełny tekst źródłaDunn, Ella, Joern R. Steinert, Aelfwin Stone, Virender Sahota, Robin S. B. Williams, Stuart Snowden i Hrvoje Augustin. "Medium-Chain Fatty Acids Rescue Motor Function and Neuromuscular Junction Degeneration in a Drosophila Model of Amyotrophic Lateral Sclerosis". Cells 12, nr 17 (28.08.2023): 2163. http://dx.doi.org/10.3390/cells12172163.
Pełny tekst źródłaBožič, Tim, Matja Zalar, Boris Rogelj, Janez Plavec i Primož Šket. "Structural Diversity of Sense and Antisense RNA Hexanucleotide Repeats Associated with ALS and FTLD". Molecules 25, nr 3 (25.01.2020): 525. http://dx.doi.org/10.3390/molecules25030525.
Pełny tekst źródłaLopez-Gonzalez, Rodrigo, Dejun Yang, Mochtar Pribadi, Tanya S. Kim, Gopinath Krishnan, So Yoen Choi, Soojin Lee, Giovanni Coppola i Fen-Biao Gao. "Partial inhibition of the overactivated Ku80-dependent DNA repair pathway rescues neurodegeneration in C9ORF72-ALS/FTD". Proceedings of the National Academy of Sciences 116, nr 19 (24.04.2019): 9628–33. http://dx.doi.org/10.1073/pnas.1901313116.
Pełny tekst źródłaBuchman, Vladimir L., Johnathan Cooper-Knock, Natalie Connor-Robson, Adrian Higginbottom, Janine Kirby, Olga D. Razinskaya, Natalia Ninkina i Pamela J. Shaw. "Simultaneous and independent detection of C9ORF72 alleles with low and high number of GGGGCC repeats using an optimised protocol of Southern blot hybridisation". Molecular Neurodegeneration 8, nr 1 (2013): 12. http://dx.doi.org/10.1186/1750-1326-8-12.
Pełny tekst źródłaMori, Kohji, Sven Lammich, Ian R. A. Mackenzie, Ignasi Forné, Sonja Zilow, Hans Kretzschmar, Dieter Edbauer i in. "hnRNP A3 binds to GGGGCC repeats and is a constituent of p62-positive/TDP43-negative inclusions in the hippocampus of patients with C9orf72 mutations". Acta Neuropathologica 125, nr 3 (5.02.2013): 413–23. http://dx.doi.org/10.1007/s00401-013-1088-7.
Pełny tekst źródłaZhang, Yuan, Christopher Roland i Celeste Sagui. "Structure and Dynamics of DNA and RNA Double Helices Obtained from the GGGGCC and CCCCGG Hexanucleotide Repeats That Are the Hallmark of C9FTD/ALS Diseases". ACS Chemical Neuroscience 8, nr 3 (19.12.2016): 578–91. http://dx.doi.org/10.1021/acschemneuro.6b00348.
Pełny tekst źródłaFreibaum, Brian D., Yubing Lu, Rodrigo Lopez-Gonzalez, Nam Chul Kim, Sandra Almeida, Kyung-Ha Lee, Nisha Badders i in. "GGGGCC repeat expansion in C9orf72 compromises nucleocytoplasmic transport". Nature 525, nr 7567 (26.08.2015): 129–33. http://dx.doi.org/10.1038/nature14974.
Pełny tekst źródłaThys, Ryan Griffin, i Yuh-Hwa Wang. "DNA Replication Dynamics of the GGGGCC Repeat of theC9orf72Gene". Journal of Biological Chemistry 290, nr 48 (13.10.2015): 28953–62. http://dx.doi.org/10.1074/jbc.m115.660324.
Pełny tekst źródłaAkimoto, Chizuru, Lars Forsgren, Jan Linder, Anna Birve, Irene Backlund, Jörgen Andersson, Ann-Charloth Nilsson, Helena Alstermark i Peter M. Andersen. "No GGGGCC-hexanucleotide repeat expansion inC9ORF72in parkinsonism patients in Sweden". Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration 14, nr 1 (17.09.2012): 26–29. http://dx.doi.org/10.3109/17482968.2012.725415.
Pełny tekst źródłaFratta, Pietro, Mark Poulter, Tammaryn Lashley, Jonathan D. Rohrer, James M. Polke, Jon Beck, Natalie Ryan i in. "Homozygosity for the C9orf72 GGGGCC repeat expansion in frontotemporal dementia". Acta Neuropathologica 126, nr 3 (2.07.2013): 401–9. http://dx.doi.org/10.1007/s00401-013-1147-0.
Pełny tekst źródłaYe, Amanda J., W. John Haynes i Daniel P. Romero. "Expression of Mutated Paramecium Telomerase RNAs In Vivo Leads to Templating Errors That Resemble Those Made by Retroviral Reverse Transcriptase". Molecular and Cellular Biology 19, nr 4 (1.04.1999): 2887–94. http://dx.doi.org/10.1128/mcb.19.4.2887.
Pełny tekst źródłaMori, K., S. M. Weng, T. Arzberger, S. May, K. Rentzsch, E. Kremmer, B. Schmid i in. "The C9orf72 GGGGCC Repeat Is Translated into Aggregating Dipeptide-Repeat Proteins in FTLD/ALS". Science 339, nr 6125 (7.02.2013): 1335–38. http://dx.doi.org/10.1126/science.1232927.
Pełny tekst źródłaZhang, Yun, Junliu Huang, Kainan Yu i Xiaojie Cui. "G-Quadruplexes Formation by the C9orf72 Nucleotide Repeat Expansion d(GGGGCC)n and Conformation Regulation by Fangchinoline". Molecules 28, nr 12 (9.06.2023): 4671. http://dx.doi.org/10.3390/molecules28124671.
Pełny tekst źródłaTseng, Yi-Ju, Siara N. Sandwith, Katelyn M. Green, Antonio E. Chambers, Amy Krans, Heather M. Raimer, Meredith E. Sharlow i in. "The RNA helicase DHX36–G4R1 modulates C9orf72 GGGGCC hexanucleotide repeat–associated translation". Journal of Biological Chemistry 297, nr 2 (sierpień 2021): 100914. http://dx.doi.org/10.1016/j.jbc.2021.100914.
Pełny tekst źródłaKonno, T., A. Shiga, A. Tsujino, A. Sugai, T. Kato, K. Kanai, A. Yokoseki i in. "Japanese amyotrophic lateral sclerosis patients with GGGGCC hexanucleotide repeat expansion in C9ORF72". Journal of Neurology, Neurosurgery & Psychiatry 84, nr 4 (25.09.2012): 398–401. http://dx.doi.org/10.1136/jnnp-2012-302272.
Pełny tekst źródłaBrčić, Jasna, i Janez Plavec. "G-quadruplex formation of oligonucleotides containing ALS and FTD related GGGGCC repeat". Frontiers of Chemical Science and Engineering 10, nr 2 (1.02.2016): 222–37. http://dx.doi.org/10.1007/s11705-016-1556-4.
Pełny tekst źródłaHe, Hua, Wen Huang, Ruoxi Wang, Yunting Lin, Yichen Guo, Jing Deng, Haitao Deng i in. "Amyotrophic Lateral Sclerosis-associated GGGGCC repeat expansion promotes Tau phosphorylation and toxicity". Neurobiology of Disease 130 (październik 2019): 104493. http://dx.doi.org/10.1016/j.nbd.2019.104493.
Pełny tekst źródłaLu, Yihuan, Chikara Dohno i Kazuhiko Nakatani. "Recognition of expanded GGGGCC hexanucleotide repeat by synthetic ligand through interhelical binding". Biochemical and Biophysical Research Communications 531, nr 1 (październik 2020): 56–61. http://dx.doi.org/10.1016/j.bbrc.2020.03.107.
Pełny tekst źródłaGoodman, Lindsey D., i Nancy M. Bonini. "Repeat-associated non-AUG (RAN) translation mechanisms are running into focus for GGGGCC-repeat associated ALS/FTD". Progress in Neurobiology 183 (grudzień 2019): 101697. http://dx.doi.org/10.1016/j.pneurobio.2019.101697.
Pełny tekst źródłaRutherford, Nicola J., Michael G. Heckman, Mariely DeJesus-Hernandez, Matt C. Baker, Alexandra I. Soto-Ortolaza, Sruti Rayaprolu, Heather Stewart i in. "Length of normal alleles of C9ORF72 GGGGCC repeat do not influence disease phenotype". Neurobiology of Aging 33, nr 12 (grudzień 2012): 2950.e5–2950.e7. http://dx.doi.org/10.1016/j.neurobiolaging.2012.07.005.
Pełny tekst źródłaZamiri, Bita, Kaalak Reddy, Christopher E. Pearson i Robert B. Macgregor. "The Structure of the Disease-Associated (GGGGCC)N Repeat from the C9ORF72 Gene". Biophysical Journal 106, nr 2 (styczeń 2014): 283a. http://dx.doi.org/10.1016/j.bpj.2013.11.1655.
Pełny tekst źródłaROMERO, DANIEL P., i ELIZABETH H. BLACKBURN. "Circular rDNA Replicons Persist in Tetrahymena thermophila Transformants Synthesizing GGGGTC Telomeric Repeats". Journal of Eukaryotic Microbiology 42, nr 1 (styczeń 1995): 32–43. http://dx.doi.org/10.1111/j.1550-7408.1995.tb01537.x.
Pełny tekst źródłaXu, Z., M. Poidevin, X. Li, Y. Li, L. Shu, D. L. Nelson, H. Li i in. "Expanded GGGGCC repeat RNA associated with amyotrophic lateral sclerosis and frontotemporal dementia causes neurodegeneration". Proceedings of the National Academy of Sciences 110, nr 19 (3.04.2013): 7778–83. http://dx.doi.org/10.1073/pnas.1219643110.
Pełny tekst źródłaGoodman, Lindsey D., Mercedes Prudencio, Nicholas J. Kramer, Luis F. Martinez-Ramirez, Ananth R. Srinivasan, Matthews Lan, Michael J. Parisi i in. "Toxic expanded GGGGCC repeat transcription is mediated by the PAF1 complex in C9orf72-associated FTD". Nature Neuroscience 22, nr 6 (20.05.2019): 863–74. http://dx.doi.org/10.1038/s41593-019-0396-1.
Pełny tekst źródłaShen, Jianying, Yu Zhang, Shi Zhao, Hong Mao, Zhongjing Wang, Honglian Li i Zihui Xu. "Purα Repaired Expanded Hexanucleotide GGGGCC Repeat Noncoding RNA-Caused Neuronal Toxicity in Neuro-2a Cells". Neurotoxicity Research 33, nr 4 (3.10.2017): 693–701. http://dx.doi.org/10.1007/s12640-017-9803-0.
Pełny tekst źródłaBrčić, Jasna, i Janez Plavec. "ALS and FTD linked GGGGCC-repeat containing DNA oligonucleotide folds into two distinct G-quadruplexes". Biochimica et Biophysica Acta (BBA) - General Subjects 1861, nr 5 (maj 2017): 1237–45. http://dx.doi.org/10.1016/j.bbagen.2016.11.018.
Pełny tekst źródłaSouza, Paulo Victor Sgobbi de, Wladimir Bocca Vieira de Rezende Pinto i Acary Souza Bulle Oliveira. "C9orf72-related disorders: expanding the clinical and genetic spectrum of neurodegenerative diseases". Arquivos de Neuro-Psiquiatria 73, nr 3 (marzec 2015): 246–56. http://dx.doi.org/10.1590/0004-282x20140229.
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