Evidence map›Paper›PMID 26824761›Full record

ArticlePloS one2016

ZMYND10--Mutation Analysis in Slavic Patients with Primary Ciliary Dyskinesia.

Małgorzata Kurkowiak, Ewa Ziętkiewicz, Agnieszka Greber, Katarzyna Voelkel, Alina Wojda, Andrzej Pogorzelski, Michał Witt

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 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 14% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Guideline
  2. A homozygous splice-site variant inFrontiers in medicine · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. PCD Genes-From Patients to Model Organisms and Back to Humans.International journal of molecular sciences · 2022
    Review
  7. Review
  8. Role of the Novel Hsp90 Co-Chaperones in Dynein Arms' Preassembly.International journal of molecular sciences · 2019
    Review
  9. Article
  10. 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

7 authors at 3 institutions in 1 country.

Małgorzata KurkowiakDepartment of Molecular and Clinical Genetics, Institute of Human Genetics, Polish Academy of Sciences, Poznań, Poland.
Ewa ZiętkiewiczDepartment of Molecular and Clinical Genetics, Institute of Human Genetics, Polish Academy of Sciences, Poznań, Poland.
Agnieszka GreberDepartment of Molecular and Clinical Genetics, Institute of Human Genetics, Polish Academy of Sciences, Poznań, Poland.
Katarzyna VoelkelDepartment of Molecular and Clinical Genetics, Institute of Human Genetics, Polish Academy of Sciences, Poznań, Poland.
Alina WojdaDepartment of Molecular and Clinical Genetics, Institute of Human Genetics, Polish Academy of Sciences, Poznań, Poland.
Andrzej PogorzelskiDepartment of Pneumology and Cystic Fibrosis, Institute of Tuberculosis and Lung Diseases, Rabka Zdrój, Poland.
Michał WittDepartment of Molecular and Clinical Genetics, Institute of Human Genetics, Polish Academy of Sciences, Poznań, Poland.
Institute of Human Genetics · PLInternational Institute of Molecular and Cell Biology · PLPolish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Primary ciliary dyskinesia (PCD) is a rare recessive disease with a prevalence of 1/10,000; its symptoms are caused by a kinetic dysfunction of motile cilia in the respiratory epithelium, flagella in spermatozoids, and primary cilia in the embryonic node. PCD is genetically heterogeneous: genotyping the already known PCD-related genes explains the genetic basis in 60-65% of the cases, depending on the population. While identification of new genes involved in PCD pathogenesis remains crucial, the search for new, population-specific mutations causative for PCD is equally important. The Slavs remain far less characterized in this respect compared to West European populations, which significantly limits diagnostic capability. The main goal of this study was to characterize the profile of causative genetic defects in one of the PCD-causing genes, ZMYND10, in the cohort of PCD patients of Slavic origin. The study was carried out using biological material from 172 unrelated PCD individuals of Polish origin, with no causative mutation found in nine major PCD genes. While none of the previously described mutations was found using the HRM-based screening, a novel frameshift mutation (c.367delC) in ZMYND10, unique for Slavic PCD population, was found in homozygous state in two unrelated PCD patients. Immunofluorescence analysis confirmed the absence of outer and inner dynein arms from the ciliary axoneme, consistent with the already published ZMYND10-mutated phenotype; cDNA analysis revealed the lack of ZMYND10 mRNA, indicating nonsense-mediated decay of the truncated transcript.

Indexed as

Frameshift MutationBase SequenceCiliaCytoskeletal ProteinsDyneinsFemaleGene ExpressionGenes, RecessiveGenetic HeterogeneityHomozygoteHumansKartagener SyndromeMaleMolecular Sequence DataPedigreePolandCytoskeletal ProteinsDyneinsRNA, MessengerTumor Suppressor ProteinsZMYND10 protein, human

Identifiers

PMID26824761
PMCPMC4732763
OpenAlexW2413498669

What OpenQuestion holds

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LicenceCC BY
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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.