Literature DB >> 26142250

Novel missense mutation of the FAM83H gene causes retention of amelogenin and a mild clinical phenotype of hypocalcified enamel.

Blanca Urzúa1, Carolina Martínez2, Ana Ortega-Pinto3, Daniela Adorno4, Irene Morales-Bozo5, Gonzalo Riadi6, Lilian Jara7, Anita Plaza8, Claudia Lefimil9, Carla Lozano10, Monserrat Reyes11.   

Abstract

OBJECTIVE: Amelogenesis imperfecta (AI) is a group of clinically and genetically heterogeneous inherited conditions, causing alterations in the structure of enamel and chemical composition of enamel matrix during development. The objective of this study was to compare the clinical, radiographic, histological and immunohistochemical phenotypes of subjects affected with hypocalcified AI from three Chilean families and identify causal mutations in the FAM83H gene.
DESIGN: The diagnosis was made using clinical, radiographic, histological and genealogical data from the patients, who were evaluated according to the classification criteria by Witkop. PCR and Sanger sequencing of the complete coding sequence and surrounding intron regions of the FAM83H gene were conducted. The structural study of the affected teeth was performed with light microscopy, scanning electron microscopy and immunohistochemistry.
RESULTS: The probands of the three families were diagnosed with hypocalcified AI, but in only one of them the missense variant p.Gly557Cys was identified. This variant was not present in the SNP database or in 100 healthy controls and segregated with the disease in the affected family. Using light microscopy, a normal prismatic structure was observed in all three cases. However, the ultrastructure was found to be affected in two of the cases, showing persistence of organic matter including amelogenins.
CONCLUSIONS: These results suggest that FAM83H missense mutation reported in one of the families analyzed in this study might cause a phenotype of hypocalcified enamel more attenuated with retention of amelogenin.
Copyright © 2015 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Amelogenesis; Amelogenin retention; FAM83H gene; Mild phenotype; Missense mutation

Mesh:

Substances:

Year:  2015        PMID: 26142250     DOI: 10.1016/j.archoralbio.2015.06.016

Source DB:  PubMed          Journal:  Arch Oral Biol        ISSN: 0003-9969            Impact factor:   2.633


  10 in total

1.  Evolutionary analysis of FAM83H in vertebrates.

Authors:  Wushuang Huang; Mei Yang; Changning Wang; Yaling Song
Journal:  PLoS One       Date:  2017-07-06       Impact factor: 3.240

2.  FAM83H and SCRIB stabilize β-catenin and stimulate progression of gastric carcinoma.

Authors:  Usama Khamis Hussein; Sang Hoon Ha; Asmaa Gamal Ahmed; Kyoung Min Kim; See-Hyoung Park; Chan Young Kim; Keun Sang Kwon; Zhongkai Zhang; Sang-A Lee; Ho Sung Park; Byung-Hyun Park; Ho Lee; Myoung Ja Chung; Woo Sung Moon; Myoung Jae Kang; Kyu Yun Jang
Journal:  Aging (Albany NY)       Date:  2020-06-20       Impact factor: 5.682

3.  The Expression Patterns of FAM83H and PANX2 Are Associated With Shorter Survival of Clear Cell Renal Cell Carcinoma Patients.

Authors:  Kyoung Min Kim; Usama Khamis Hussein; Jun Sang Bae; See-Hyoung Park; Keun Sang Kwon; Sang Hoon Ha; Ho Sung Park; Ho Lee; Myoung Ja Chung; Woo Sung Moon; Myoung Jae Kang; Kyu Yun Jang
Journal:  Front Oncol       Date:  2019-01-22       Impact factor: 6.244

4.  The Enamel Phenotype in Homozygous Fam83h Truncation Mice.

Authors:  Shih-Kai Wang; Yuanyuan Hu; Charles E Smith; Jie Yang; Chunhua Zeng; Jung-Wook Kim; Jan C-C Hu; James P Simmer
Journal:  Mol Genet Genomic Med       Date:  2019-05-06       Impact factor: 2.183

5.  FAM83H and Nectin1 expression are related with survival and relapse of bladder urothelial carcinoma patients.

Authors:  Ae-Ri Ahn; Sang Jae Noh; Usama Khamis Hussein; Ho Sung Park; Myoung Ja Chung; Ho Lee; Woo Sung Moon; Myoung Jae Kang; Hyung Jin Kim; Na Ri Lee; Kyu Yun Jang; Kyoung Min Kim
Journal:  BMC Urol       Date:  2021-10-08       Impact factor: 2.264

6.  An Intron c.103-3T>C Variant of the AMELX Gene Causes Combined Hypomineralized and Hypoplastic Type of Amelogenesis Imperfecta: Case Series and Review of the Literature.

Authors:  Tina Leban; Katarina Trebušak Podkrajšek; Jernej Kovač; Aleš Fidler; Alenka Pavlič
Journal:  Genes (Basel)       Date:  2022-07-18       Impact factor: 4.141

7.  FAM83H and casein kinase I regulate the organization of the keratin cytoskeleton and formation of desmosomes.

Authors:  Takahisa Kuga; Mitsuho Sasaki; Toshinari Mikami; Yasuo Miake; Jun Adachi; Maiko Shimizu; Youhei Saito; Minako Koura; Yasunori Takeda; Junichiro Matsuda; Takeshi Tomonaga; Yuji Nakayama
Journal:  Sci Rep       Date:  2016-05-25       Impact factor: 4.379

8.  Novel FAM83H mutations in patients with amelogenesis imperfecta.

Authors:  Wang Xin; Wang Wenjun; Qin Man; Zhao Yuming
Journal:  Sci Rep       Date:  2017-07-20       Impact factor: 4.379

9.  Characterisation of the biochemical and cellular roles of native and pathogenic amelogenesis imperfecta mutants of FAM83H.

Authors:  Theresa Tachie-Menson; Ana Gázquez-Gutiérrez; Luke J Fulcher; Thomas J Macartney; Nicola T Wood; Joby Varghese; Robert Gourlay; Renata F Soares; Gopal P Sapkota
Journal:  Cell Signal       Date:  2020-04-11       Impact factor: 4.315

Review 10.  The FAM83 family of proteins: from pseudo-PLDs to anchors for CK1 isoforms.

Authors:  Polyxeni Bozatzi; Gopal P Sapkota
Journal:  Biochem Soc Trans       Date:  2018-06-05       Impact factor: 5.407

  10 in total

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