Evidence map›Paper›PMID 27128441›Full record

ArticlePloS one2016

Manipulating the Prion Protein Gene Sequence and Expression Levels with CRISPR/Cas9.

Lech Kaczmarczyk, Ylva Mende, Branko Zevnik, Walker S Jackson

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Prion diseases: Lessons from historical outbreaks and potential emerging ones.Protein science : a publication of the Protein Society · 2025
    Review
  2. Article
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  4. Article
  5. Article
  6. Review
  7. Genetic aspects of human prion diseases.Frontiers in neurology · 2022
    Review
  8. Review
  9. Article
  10. Article
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  13. Next Generation Precision Medicine: CRISPR-mediated Genome Editing for the Treatment of Neurodegenerative Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
    Review
  14. Article
  15. Article
  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Lech KaczmarczykGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Ylva MendeCologne Excellence Cluster on Cellular Stress Responses in Aging-associated Diseases (CECAD), Medical Faculty, University of Cologne, Cologne, Germany.
Branko ZevnikCologne Excellence Cluster on Cellular Stress Responses in Aging-associated Diseases (CECAD), Medical Faculty, University of Cologne, Cologne, Germany.
Walker S JacksonGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEGerman Center for Neurodegenerative Diseases · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

CRISPR-Cas SystemsAnimalsCell LineFemaleGene ExpressionGene Knock-In TechniquesGene TargetingGenetic VectorsHumansMaleMiceMice, Inbred C57BLMice, KnockoutPrion DiseasesPrion ProteinsUp-RegulationPrion ProteinsPrnp protein, mouse

Identifiers

PMID27128441
PMCPMC4851410
OpenAlexW2344327571

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.