Evidence map›Paper›PMID 37077890›Full record

ArticleFrontiers in genome editing2023

CRISPR/Cas9-generated mouse model with humanizing single-base substitution in the

Anna V Polikarpova, Tatiana V Egorova, Evgenii A Lunev, Alexandra A Tsitrina, Svetlana G Vassilieva, Irina M Savchenko, Yuliya Y Silaeva, Alexey V Deykin, Maryana V Bardina

Open access · goldAbstract read
In one paragraph

Article in Frontiers in genome editing, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Decoding GNAO1 mutations usingFrontiers in cellular neuroscience · 2025
    Review
  6. CRISPR/Cas9 as a Mutagenic Factor.International journal of molecular sciences · 2024
    Review
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 2 countries.

Anna V PolikarpovaLaboratory of Modeling and Gene Therapy of Hereditary Diseases, Institute of Gene Biology Russian Academy of Sciences, Moscow, Russia.
Tatiana V EgorovaLaboratory of Modeling and Gene Therapy of Hereditary Diseases, Institute of Gene Biology Russian Academy of Sciences, Moscow, Russia.
Evgenii A LunevLaboratory of Modeling and Gene Therapy of Hereditary Diseases, Institute of Gene Biology Russian Academy of Sciences, Moscow, Russia.
Alexandra A TsitrinaKoltzov Institute of Developmental Biology Russian Academy of Sciences, Moscow, Russia.
Svetlana G VassilievaLaboratory of Modeling and Gene Therapy of Hereditary Diseases, Institute of Gene Biology Russian Academy of Sciences, Moscow, Russia.
Irina M SavchenkoMarlin Biotech, Sochi, Russia.
Yuliya Y SilaevaCore Facility Center, Institute of Gene Biology Russian Academy of Sciences, Moscow, Russia.
Alexey V DeykinMarlin Biotech, Sochi, Russia.
Maryana V BardinaLaboratory of Modeling and Gene Therapy of Hereditary Diseases, Institute of Gene Biology Russian Academy of Sciences, Moscow, Russia.
Institute of Gene Biology · RUSochi State University · RUKoltzov Institute of Developmental Biology · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of personalized medicine for genetic diseases requires preclinical testing in the appropriate animal models. GNAO1 encephalopathy is a severe neurodevelopmental disorder caused by heterozygous

Indexed as

CRISPR/Cas9genetically modified micegenome editingGNAO1 encephalopathypersonalized medicine

Identifiers

PMID37077890
PMCPMC10106585
OpenAlexW4362585281

What OpenQuestion holds

Textmetadata
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.