Evidence map›Paper›PMID 30985756›Full record

ArticleJournal of visualized experiments : JoVE2019

Lentiviral Vector Platform for the Efficient Delivery of Epigenome-editing Tools into Human Induced Pluripotent Stem Cell-derived Disease Models.

Lidia Tagliafierro, Ekaterina Ilich, Malik Moncalvo, Jeffrey Gu, Ahila Sriskanda, Carole Grenier, Susan K Murphy, Ornit Chiba-Falek, Boris Kantor

Open access · greenAbstract readVideo-Audio Media
In one paragraph

Article in Journal of visualized experiments : JoVE, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

14 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
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  3. Review
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  5. CRB2 depletion induces YAP signaling and disrupts mechanosensing in podocytes.American journal of physiology. Renal physiology · 2025
    Article
  6. Neuronal-type-specific epigenome editing to decreaseMolecular therapy. Nucleic acids · 2024
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
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  13. Article
  14. 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

9 authors at 3 institutions in 1 country.

Lidia TagliafierroDepartment of Neurology, Duke University Medical Center; Center for Genomic and Computational Biology, Duke University Medical Center.
Ekaterina IlichViral Vector Core, Duke University Medical Center.
Malik MoncalvoViral Vector Core, Duke University Medical Center.
Jeffrey GuDepartment of Neurology, Duke University Medical Center.
Ahila SriskandaDepartment of Neurology, Duke University Medical Center; Center for Genomic and Computational Biology, Duke University Medical Center.
Carole GrenierDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, Duke University Medical Center.
Susan K MurphyDivision of Gynecologic Oncology, Department of Obstetrics and Gynecology, Duke University Medical Center.
Ornit Chiba-FalekDepartment of Neurology, Duke University Medical Center; Center for Genomic and Computational Biology, Duke University Medical Center; o.chibafalek@duke.edu.
Boris KantorViral Vector Core, Duke University Medical Center; boris.kantor@duke.edu.
Duke Medical Center · USDuke University Hospital · USVector (United States) · US

Funding

Lewy body neuropathologies and SNCA gene: variants expression and splicingR01NS085011 · NINDS · DUKE UNIVERSITY · PI CHIBA-FALEK, ORNIT · 2013 to 2017
$1.8M
NINDS NIH HHS R01 NS085011
6 · The paper itself

Abstract

The use of hiPSC-derived cells represents a valuable approach to study human neurodegenerative diseases. Here, we describe an optimized protocol for the differentiation of hiPSCs derived from a patient with the triplication of the alpha-synuclein gene (SNCA) locus into Parkinson's disease (PD)-relevant dopaminergic neuronal populations. Accumulating evidence has shown that high levels of SNCA are causative for the development of PD. Recognizing the unmet need to establish novel therapeutic approaches for PD, especially those targeting the regulation of SNCA expression, we recently developed a CRISPR/dCas9-DNA-methylation-based system to epigenetically modulate SNCA transcription by enriching methylation levels at the SNCA intron 1 regulatory region. To deliver the system, consisting of a dead (deactivated) version of Cas9 (dCas9) fused with the catalytic domain of the DNA methyltransferase enzyme 3A (DNMT3A), a lentiviral vector is used. This system is applied to cells with the triplication of the SNCA locus and reduces the SNCA-mRNA and protein levels by about 30% through the targeted DNA methylation of SNCA intron 1. The fine-tuned downregulation of the SNCA levels rescues disease-related cellular phenotypes. In the current protocol, we aim to describe a step-by-step procedure for differentiating hiPSCs into neural progenitor cells (NPCs) and the establishment and validation of pyrosequencing assays for the evaluation of the methylation profile in the SNCA intron 1. To outline in more detail the lentivirus-CRISPR/dCas9 system used in these experiments, this protocol describes how to produce, purify, and concentrate lentiviral vectors and to highlight their suitability for epigenome- and genome-editing applications using hiPSCs and NPCs. The protocol is easily adaptable and can be used to produce high titer lentiviruses for in vitro and in vivo applications.

Indexed as

Cell DifferentiationEpigenomeEpigenomicsGene EditingHumansInduced Pluripotent Stem CellsLentivirus

Identifiers

PMID30985756
PMCPMC7144461
OpenAlexW2935082840

What OpenQuestion holds

Textmetadata
LicenceTDM
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.