ArticleMeta gene2014
Keratin 13 mutations associated with oral white sponge nevus in two Chinese families.
Article in Meta gene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- KRT13 Drives Pancreatic Cancer Malignancy Via the PI3K/AKT-PPARG Axis While Enhancing Sensitivity to Navitoclax.Medical science monitor : international medical journal of experimental and clinical research · 2026Article
- Innovative Combination of Tetracycline Rinse and CO₂ Laser Ablation for Treating White Sponge Nevus in Adolescents: A Case Study.The American journal of case reports · 2024Article
- Article
- Identification of Potentially Pathogenic Variants Associated with Recurrence in Medication-Related Osteonecrosis of the Jaw (MRONJ) Patients Using Whole-Exome Sequencing.Journal of clinical medicine · 2022Article
- Keratin 13 Is Enriched in Prostate Tubule-Initiating Cells and May Identify Primary Prostate Tumors that Metastasize to the Bone.PloS one · 2016Article
- Expression profiling of white sponge nevus by RNA sequencing revealed pathological pathways.Orphanet journal of rare diseases · 2015Article
- White sponge nevus: Report of three cases in a single family.Journal of oral and maxillofacial pathology : JOMFPArticle
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
White sponge nevus (WSN) is an autosomal dominant hereditary disease. Keratin 4 (KRT4) and Keratin 13 (KRT13) gene mutations were involved in the WSN. We recruited two WSN Chinese families, and oral lesion biopsy with hematoxylin and eosin staining showed that patients had significant pathological characteristics. The mutations of KRT4 and KRT13 gene were detected by PCR and direct sequencing. The multiple alignments of KRT13 from 23 diverse species homology analyses were performed by the ClustalW program. The KRT13 expression was measured by Real-Time RT-PCR and Western blot analysis. Sequencing analysis revealed two mutations of KRT13 gene: one mutation was 332T>C and amino acid change was Leu111Pro. Another mutation was 340C>T and amino acid change was Arg114Cys. The sequence of KRT13 was highly conserved. Real-Time RT-PCR and Western blot analysis results show that KRT13 expression level is lower in patient but keep almost no change in mRNA level. When cells were treated with MG132, KRT13 protein level was increased and kept almost the same in normal and patient cells. We identified two heritable mutations in the KRT13 gene, which were associated with the development of WSN. The abnormal degradation of KRT13 protein of WSN may probably associate with the abnormal ubiquitination process.
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