Evidence map›Paper›PMID 34669720›Full record

ArticlePloS one2021

Expanding the clinical phenotype associated with NIPAL4 mutation: Study of a Tunisian consanguineous family with erythrokeratodermia variabilis-Like Autosomal Recessive Congenital Ichthyosis.

Cherine Charfeddine, Nadia Laroussi, Rahma Mkaouar, Raja Jouini, Olfa Khayat, Aladin Redissi, Amor Mosbah, Hamza Dallali, Achraf Chedly Debbiche, Anissa Zaouak and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

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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

13 authors at 3 institutions in 1 country.

Cherine CharfeddineUniversity Tunis El Manar, Institut Pasteur de Tunis, Biomedical Genomics and Oncogenetics Laboratory, LR20IPT05, Tunis, Tunisia.ORCID 0000-0002-4656-2661
Nadia LaroussiUniversity Tunis El Manar, Institut Pasteur de Tunis, Biomedical Genomics and Oncogenetics Laboratory, LR20IPT05, Tunis, Tunisia.
Rahma MkaouarUniversity Tunis El Manar, Institut Pasteur de Tunis, Biomedical Genomics and Oncogenetics Laboratory, LR20IPT05, Tunis, Tunisia.
Raja JouiniDepartment of Pathology, Habib Thameur Hospital, Tunis, Tunisia.
Olfa KhayatDepartment of Pathology, Habib Thameur Hospital, Tunis, Tunisia.
Aladin RedissiBVBGR-LR11ES31, ISBST, Université de la Manouba, Institut de Biotechnologie de Sidi Thabet, Ariana, Tunisia.
Amor MosbahBVBGR-LR11ES31, ISBST, Université de la Manouba, Institut de Biotechnologie de Sidi Thabet, Ariana, Tunisia.
Hamza DallaliUniversity Tunis El Manar, Institut Pasteur de Tunis, Biomedical Genomics and Oncogenetics Laboratory, LR20IPT05, Tunis, Tunisia.
Achraf Chedly DebbicheDepartment of Pathology, Habib Thameur Hospital, Tunis, Tunisia.
Anissa ZaouakDepartment of Dermatology, Genodermatosis and Cancers Laboratory LR12SP03, Habib Thameur Hospital, Tunis, Tunisia.
Sami FennicheDepartment of Dermatology, Genodermatosis and Cancers Laboratory LR12SP03, Habib Thameur Hospital, Tunis, Tunisia.
Sonia AbdelhakUniversity Tunis El Manar, Institut Pasteur de Tunis, Biomedical Genomics and Oncogenetics Laboratory, LR20IPT05, Tunis, Tunisia.
Houda Hammami-GhorbelDepartment of Dermatology, Genodermatosis and Cancers Laboratory LR12SP03, Habib Thameur Hospital, Tunis, Tunisia.
Habib hospital Thameur · TNInstitut Pasteur de Tunis · TNManouba University · TN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Erythrokeratodermia variabilis (EKV) is a rare disorder of cornification usually associated with dominant mutations in the GJB3 and GJB4 genes encoding connexins (Cx)31 and 30.3. Genetic heterogeneity of EKV has already been suggested. We investigated at the clinical and genetic level a consanguineous Tunisian family with 2 sisters presenting an autosomal recessive form of EKV to better characterize this disease. Mutational analysis initially screened the connexin genes and Whole-exome sequencing (WES) was performed to identify the molecular aetiology of the particular EKV phenotype in the proband. Migratory shaped erythematous areas are the initial presenting sign followed by relatively stable hyperkeratotic plaques are the two predominates characteristics in both patients. However, remarkable variability of morphological and dominating features of the disease were observed between patients. In particular, the younger sister (proband) exhibited ichthyosiform-like appearance suggesting Autosomal Recessive Congenital Ichthyosis (ARCI) condition. No causative mutations were detected in the GJB3 and GJB4 genes. WES results revealed a novel missense homozygous mutation in NIPAL4 gene (c.835C>G, p.Pro279Ala) in both patients. This variant is predicted to be likely pathogenic. In addition, in silico analysis of the mutated 3D domain structure predicted that this variant would result in NIPA4 protein destabilization and Mg2+ transport perturbation, pointing out the potential role of NIPAL4 gene in the development and maintenance of the barrier function of the epidermis. Taken togheter, these results expand the clinical phenotype associated with NIPAL4 mutation and reinforce our hypothesis of NIPAL4 as the main candidate gene for the EKV-like ARCI phenotype.

Indexed as

Mutation, MissenseChildConnexinsConsanguinityErythrokeratodermia VariabilisExome SequencingFemaleHumansInfantMolecular Docking SimulationPedigreePhenotypeProtein StabilityReceptors, Cell SurfaceTunisiaconnexin 30.3ConnexinsGJB3 protein, humanNIPAL4 protein, humanReceptors, Cell Surface

Identifiers

PMID34669720
PMCPMC8528321
OpenAlexW3206308296

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Registered trials

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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.