ArticleScientific reports2016
FAM83H and casein kinase I regulate the organization of the keratin cytoskeleton and formation of desmosomes.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Multiomics Data Synthesis of FAM83H in Amelogenesis Imperfecta.International dental journal · 2026Pooled it
- Desmoglein-driven dynamic signaling in pemphigus vulgaris: a systematic review of pathogenic pathways.NPJ Regenerative medicine · 2025Article
- FNDC3B promotes gastric cancer metastasis via interacting with FAM83H and preventing its proteasomal degradation.Cellular & molecular biology letters · 2025Article
- The DUF1669 domain of FAM83H is required for its localization to nuclear speckles.Scientific reports · 2025Article
- Expression ofInternational journal of molecular sciences · 2025Article
- Zebrafish reveal new roles for Fam83f in hatching and the DNA damage-mediated autophagic response.Open biology · 2024Article
- Notch1 cortical signaling regulates epithelial architecture and cell-cell adhesion.The Journal of cell biology · 2023Article
- Notch1 cortical signaling regulates epithelial architecture and cell-cell adhesion.bioRxiv : the preprint server for biology · 2023Article
- Article
- CRISPR/Cas9-mediated deletion of Fam83h induces defective tooth mineralization and hair development in rabbits.Journal of cellular and molecular medicine · 2022Article
- The conserved C-terminal residues of FAM83H are required for the recruitment of casein kinase 1 to the keratin cytoskeleton.Scientific reports · 2022Article
- Article
- Functions and regulation of the serine/threonine protein kinase CK1 family: moving beyond promiscuity.The Biochemical journal · 2020Review
- FAM83H overexpression predicts worse prognosis and correlates with less CD8Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Article
- Expression of FAM83H and ZNF16 are associated with shorter survival of patients with gallbladder carcinoma.Diagnostic pathology · 2020Article
- RNA-seq analysis identifies cytoskeletal structural genes and pathways for meat quality in beef.PloS one · 2020Article
- Decreased osteogenic activity and mineralization of alveolar bone cells from a patient with amelogenesis imperfecta andGenes & diseases · 2019Article
- Family with Sequence Similarity 83 Member H Promotes the Viability and Metastasis of Cervical Cancer Cells and Indicates a Poor Prognosis.Yonsei medical journal · 2019Article
- Long non-coding RNA FAM83H-AS1 is regulated by human papillomavirus 16 E6 independently of p53 in cervical cancer cells.Scientific reports · 2019Article
- Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FAM83H is essential for the formation of dental enamel because a mutation in the FAM83H gene causes amelogenesis imperfecta (AI). We previously reported that the overexpression of FAM83H often occurs and disorganizes the keratin cytoskeleton in colorectal cancer cells. We herein show that FAM83H regulates the organization of the keratin cytoskeleton and maintains the formation of desmosomes in ameloblastoma cells. FAM83H is expressed and localized on keratin filaments in human ameloblastoma cell lines and in mouse ameloblasts and epidermal germinative cells in vivo. FAM83H shows preferential localization to keratin filaments around the nucleus that often extend to cell-cell junctions. Alterations in the function of FAM83H by its overexpression, knockdown, or an AI-causing truncated mutant prevent the proper organization of the keratin cytoskeleton in ameloblastoma cells. Furthermore, the AI-causing mutant prevents desmosomal proteins from being localized to cell-cell junctions. The effects of the AI-causing mutant depend on its binding to and possible inhibition of casein kinase I (CK-1). The suppression of CK-1 by its inhibitor, D4476, disorganizes the keratin cytoskeleton. Our results suggest that AI caused by the FAM83H mutation is mediated by the disorganization of the keratin cytoskeleton and subsequent disruption of desmosomes in ameloblasts.
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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.