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Department of Biology Faculty of Medi... 1 Department of Biology Faculty of Medi... 1 Department of Biology Faculty of Medi... 1 Department of Biology Faculty of Medi... 1 Department of Biology Faculty of Medi... 1 International Clinical Research Cente... 1 PhyMedExp INSERM University of Montpe... 1
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Department of Biology Faculty of Medi... 1 Department of Biology Faculty of Medi... 1 Department of Biology Faculty of Medi... 1 Department of Biology Faculty of Medi... 1 Department of Biology Faculty of Medi... 1 International Clinical Research Cente... 1 PhyMedExp INSERM University of Montpe... 1
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- Jelinkova, Sarka
- Fojtik, Petr
- Kohutova, Aneta
- Vilotic, Aleksandra
- Marková, Lenka
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Pesl, Martin
Autor Pesl, Martin Department of Biology, Faculty of Medicine, Masaryk University, 625 00 Brno, Czech Republic. peslmartin@gmail.com. International Clinical Research Center ICRC, St. Anne's University Hospital Brno, 602 00 Brno, Czech Republic. peslmartin@gmail.com. 1st department of Internal Medicine-Cardioangiology, Faculty of Medicine, Masaryk University, 602 00 Brno, Czech Republic. peslmartin@gmail.com
- Jurakova, Tereza
- Kruta, Miriama
- Vrbsky, Jan
- Gaillyova, Renata
Free Medical Journals od 2012
PubMed Central od 2012
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ProQuest Central od 2012-03-01
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PubMed
30650618
DOI
10.3390/cells8010053
Knihovny.cz E-zdroje
Recent data on Duchenne muscular dystrophy (DMD) show myocyte progenitor's involvement in the disease pathology often leading to the DMD patient's death. The molecular mechanism underlying stem cell impairment in DMD has not been described. We created dystrophin-deficient human pluripotent stem cell (hPSC) lines by reprogramming cells from two DMD patients, and also by introducing dystrophin mutation into human embryonic stem cells via CRISPR/Cas9. While dystrophin is expressed in healthy hPSC, its deficiency in DMD hPSC lines induces the release of reactive oxygen species (ROS) through dysregulated activity of all three isoforms of nitric oxide synthase (further abrev. as, NOS). NOS-induced ROS release leads to DNA damage and genomic instability in DMD hPSC. We were able to reduce both the ROS release as well as DNA damage to the level of wild-type hPSC by inhibiting NOS activity.
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Po ukončení testovacího provozu bude odkaz přesměrován adresu produkční verze portálu Medvik.