Evidence map›Paper›PMID 27292199›Full record

ArticleScientific reports2016

FAM20A binds to and regulates FAM20C localization.

Yoshio Ohyama, Ju-Hsien Lin, Nattanan Govitvattana, I-Ping Lin, Sundharamani Venkitapathi, Ahmed Alamoudi, Dina Husein, Chunying An, Hak Hotta, Masaru Kaku and 1 more

Open access · goldAbstract read
In one paragraph

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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  5. Frontiers in immunology · 2024
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  6. Review
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  8. Article
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  11. Proteolytic processing of secretory pathway kinase Fam20C by site-1 protease promotes biomineralization.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  12. Article
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  15. Article
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  18. Prospects for pharmacological targeting of pseudokinases.Nature reviews. Drug discovery · 2019
    Review
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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

11 authors at 4 institutions in 3 countries.

Yoshio OhyamaDepartment of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, Boston University, Boston, United States of America.
Ju-Hsien LinDepartment of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, Boston University, Boston, United States of America.
Nattanan GovitvattanaDepartment of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, Boston University, Boston, United States of America.
I-Ping LinDepartment of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, Boston University, Boston, United States of America.
Sundharamani VenkitapathiDepartment of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, Boston University, Boston, United States of America.
Ahmed AlamoudiDepartment of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, Boston University, Boston, United States of America.
Dina HuseinDepartment of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, Boston University, Boston, United States of America.
Chunying AnDivision of Microbiology, Kobe University Graduate School of Medicine, Kobe, Japan.
Hak HottaDivision of Microbiology, Kobe University Graduate School of Medicine, Kobe, Japan.
Masaru KakuDivision of Bio-Prosthodontics, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Yoshiyuki MochidaDepartment of Molecular and Cell Biology, Henry M. Goldman School of Dental Medicine, Boston University, Boston, United States of America.
Boston University · USKobe University · JPChulalongkorn University · THNiigata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the Family with sequence similarity (FAM) 20 gene family are associated with mineralized tissue phenotypes in humans. Among these genes, FAM20A mutations are associated with Amelogenesis Imperfecta (AI) with gingival hyperplasia and nephrocalcinosis, while FAM20C mutations cause Raine syndrome, exhibiting bone and craniofacial/dental abnormalities. Although it has been demonstrated that Raine syndrome associated-FAM20C mutants prevented FAM20C kinase activity and secretion, overexpression of the catalytically inactive D478A FAM20C mutant was detected in both cell extracts and the media. This suggests that FAM20C secretion doesn't require its kinase activity, and that another molecule(s) may control the secretion. In this study, we found that extracellular FAM20C localization was increased when wild-type (WT), but not AI-forms of FAM20A was co-transfected. On the other hand, extracellular FAM20C was absent in the conditioned media of mouse embryonic fibroblasts (MEFs) derived from Fam20a knock-out (KO) mouse, while it was detected in the media from WT MEFs. We also showed that cells with the conditioned media of Fam20a WT MEFs mineralized, but those with the conditioned media of KO MEFs failed to mineralize in vitro. Our data thus demonstrate that FAM20A controls FAM20C localization that may assist in the extracellular function of FAM20C in mineralized tissues.

Identifiers

PMID27292199
PMCPMC4904241
OpenAlexW2435596766

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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.