Home > Publications Database > Manipulating the Prion Protein Gene Sequence and Expression Levels with CRISPR/Cas9. > print

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024 7 _ |a 10.1371/journal.pone.0154604
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037 _ _ |a DZNE-2020-04868
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Kaczmarczyk, Lech
|0 P:(DE-2719)2810486
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|u dzne
245 _ _ |a Manipulating the Prion Protein Gene Sequence and Expression Levels with CRISPR/Cas9.
260 _ _ |a San Francisco, California, US
|c 2016
|b PLOS
264 _ 1 |3 online
|2 Crossref
|b Public Library of Science (PLoS)
|c 2016-04-29
336 7 _ |a article
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336 7 _ |a Output Types/Journal article
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336 7 _ |a Journal Article
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336 7 _ |a ARTICLE
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336 7 _ |a Journal Article
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520 _ _ |a The mammalian prion protein (PrP, encoded by Prnp) is most infamous for its central role in prion diseases, invariably fatal neurodegenerative diseases affecting humans, food animals, and animals in the wild. However, PrP is also hypothesized to be an important receptor for toxic protein conformers in Alzheimer's disease, and is associated with other clinically relevant processes such as cancer and stroke. Thus, key insights into important clinical areas, as well as into understanding PrP functions in normal physiology, can be obtained from studying transgenic mouse models and cell culture systems. However, the Prnp locus is difficult to manipulate by homologous recombination, making modifications of the endogenous locus rarely attempted. Fortunately in recent years genome engineering technologies, like TALENs or CRISPR/Cas9 (CC9), have brought exceptional new possibilities for manipulating Prnp. Herein, we present our observations made during systematic experiments with the CC9 system targeting the endogenous mouse Prnp locus, to either modify sequences or to boost PrP expression using CC9-based synergistic activation mediators (SAMs). It is our hope that this information will aid and encourage researchers to implement gene-targeting techniques into their research program.
536 _ _ |a 342 - Disease Mechanisms and Model Systems (POF3-342)
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542 _ _ |i 2016-04-29
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|u http://creativecommons.org/licenses/by/4.0/
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Prion Proteins
|2 NLM Chemicals
650 _ 7 |a Prnp protein, mouse
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a CRISPR-Cas Systems
|2 MeSH
650 _ 2 |a Cell Line
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Gene Expression
|2 MeSH
650 _ 2 |a Gene Knock-In Techniques: methods
|2 MeSH
650 _ 2 |a Gene Targeting: methods
|2 MeSH
650 _ 2 |a Genetic Vectors
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Mice, Inbred C57BL
|2 MeSH
650 _ 2 |a Mice, Knockout
|2 MeSH
650 _ 2 |a Prion Diseases: genetics
|2 MeSH
650 _ 2 |a Prion Proteins: genetics
|2 MeSH
650 _ 2 |a Up-Regulation
|2 MeSH
700 1 _ |a Mende, Ylva
|0 P:(DE-HGF)0
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700 1 _ |a Zevnik, Branko
|b 2
700 1 _ |a Jackson, Walker S
|0 P:(DE-2719)2810253
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773 1 8 |a 10.1371/journal.pone.0154604
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|v 11
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773 _ _ |a 10.1371/journal.pone.0154604
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856 4 _ |y OpenAccess
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856 4 _ |y OpenAccess
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856 7 _ |2 Pubmed Central
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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913 1 _ |a DE-HGF
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