Evidence map›Paper›PMID 34069872›Full record

ArticleInternational journal of molecular sciences2021

Generation and Characterization of a CRISPR/Cas9-Mediated

Marie Christine Martens, Janin Edelkamp, Christina Seebode, Mirijam Schäfer, Susanne Stählke, Saskia Krohn, Ole Jung, Hugo Murua Escobar, Steffen Emmert, Lars Boeckmann

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Loss of SP-A in the Lung Exacerbates Pulmonary Fibrosis.International journal of molecular sciences · 2022
    Article
  5. Article
  6. Review
  7. 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

10 authors at 1 institution in 1 country.

Marie Christine MartensClinic and Policlinic for Dermatology and Venerology, University Medical Center Rostock, 18057 Rostock, Germany.
Janin EdelkampClinic and Policlinic for Dermatology and Venerology, University Medical Center Rostock, 18057 Rostock, Germany.
Christina SeebodeClinic and Policlinic for Dermatology and Venerology, University Medical Center Rostock, 18057 Rostock, Germany.
Mirijam SchäferClinic and Policlinic for Dermatology and Venerology, University Medical Center Rostock, 18057 Rostock, Germany.ORCID 0000-0002-7383-3092
Susanne StählkeDepartment of Cell Biology, University Medical Center Rostock, 18057 Rostock, Germany.ORCID 0000-0002-0251-8263
Saskia KrohnClinic for Hematology, Oncology and Palliative Care, University Medical Center Rostock, 18057 Rostock, Germany.
Ole JungClinic and Policlinic for Dermatology and Venerology, University Medical Center Rostock, 18057 Rostock, Germany.
Hugo Murua EscobarClinic for Hematology, Oncology and Palliative Care, University Medical Center Rostock, 18057 Rostock, Germany.ORCID 0000-0001-7123-7986
Steffen EmmertClinic and Policlinic for Dermatology and Venerology, University Medical Center Rostock, 18057 Rostock, Germany.
Lars BoeckmannClinic and Policlinic for Dermatology and Venerology, University Medical Center Rostock, 18057 Rostock, Germany.ORCID 0000-0003-0098-6546
University of Rostock · DE

Funding

Damp Stiftung 2017-05Deutsche Forschungsgemeinschaft DFG EM 63/13-1Deutsche Stiftung Dermatologie Hiwi-Stipendium 2017European Social Fund ESF/14-BM-A55-0001/18Forschungsförderung der Universitätsmedizin Rostock FORUN
6 · The paper itself

Abstract

Loss-of-function mutations in the synaptosomal-associated protein 29 (SNAP29) lead to the rare autosomal recessive neurocutaneous cerebral dysgenesis, neuropathy, ichthyosis, and keratoderma (CEDNIK) syndrome. SNAP29 is a soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) protein. So far, it has been shown to be involved in membrane fusion, epidermal differentiation, formation of primary cilia, and autophagy. Recently, we reported the successful generation of two mouse models for the human CEDNIK syndrome. The aim of this investigation was the generation of a CRISPR/Cas9-mediated

Indexed as

AnimalsAutophagyCell DifferentiationCell LineCRISPR-Cas SystemsFibroblastsGene Knockout TechniquesHumansKeratoderma, PalmoplantarMembrane FusionMutationNeurocutaneous SyndromesQb-SNARE ProteinsQc-SNARE ProteinsSNARE ProteinsQb-SNARE ProteinsQc-SNARE ProteinsSNAP29 protein, humanSNARE ProteinsCEDNIK syndromeCRISPR/Cas9ichthyosislentiviral transductionSNAP29

Identifiers

PMID34069872
PMCPMC8157373
OpenAlexW3160944402

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.