Evidence map›Paper›PMID 18390542›Full record

ArticleThe Journal of biological chemistry2008

Partial rescue of the amelogenin null dental enamel phenotype.

Yong Li, Cynthia Suggs, J Timothy Wright, Zhi-an Yuan, Melissa Aragon, Hanson Fong, Darrin Simmons, Bill Daly, Ellis E Golub, Gerald Harrison and 2 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. 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
3.4field-weighted citation impact, top 9% 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, 30 citations in OpenAlex.

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  16. An amelogenin mutation leads to disruption of the odontogenic apparatus and aberrant expression of Notch1.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2011
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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

12 authors at 4 institutions in 1 country.

Yong LiDepartment of Anatomy and Cell Biology, University of Pennsylvania School of Dental Medicine, 240 S. 40th Street, Philadelphia, PA 19104-6030, USA.
Cynthia Suggs
J Timothy Wright
Zhi-an Yuan
Melissa Aragon
Hanson Fong
Darrin Simmons
Bill Daly
Ellis E Golub
Gerald Harrison
Ashok B Kulkarni
Carolyn W Gibson
University of Pennsylvania · USUniversity of North Carolina at Chapel Hill · USNational Institute of Dental and Craniofacial Research · USUniversity of Washington · US

Funding

ENAMEL MINERAL FORMATION DURING MURINE ODONTOGENESISR01DE011089 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI GIBSON, CAROLYN · 1995 to 2012
$3.9M
Molecular Genetics of Tooth Development and DiseaseZ01DE000698 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI KULKARNI, ASHOK B. · 1999 to 2008
$1.7M
Molecular Genetics of Craniofacial Development and DiseaseZIADE000698 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI KULKARNI, ASHOK · 2009 to 2010
$480k
NIDCR NIH HHS DE 011089NIDCR NIH HHS R01 DE011089
6 · The paper itself

Abstract

The amelogenins are the most abundant secreted proteins in developing dental enamel. Enamel from amelogenin (Amelx) null mice is hypoplastic and disorganized, similar to that observed in X-linked forms of the human enamel defect amelogenesis imperfecta resulting from amelogenin gene mutations. Both transgenic strains that express the most abundant amelogenin (TgM180) have relatively normal enamel, but strains of mice that express a mutated amelogenin (TgP70T), which leads to amelogenesis imperfecta in humans, have heterogeneous enamel structures. When Amelx null (KO) mice were mated with transgenic mice that produce M180 (TgM180), the resultant TgM180KO offspring showed evidence of rescue in enamel thickness, mineral density, and volume in molar teeth. Rescue was not observed in the molars from the TgP70TKO mice. It was concluded that a single amelogenin protein was able to significantly rescue the KO phenotype and that one amino acid change abrogated this function during development.

Indexed as

AmelogeninAmino Acid SubstitutionAnimalsDental EnamelDental Enamel HypoplasiaHumansMiceMice, KnockoutMolarOrgan SizeAmelogenin

Identifiers

PMID18390542
PMCPMC2397487
OpenAlexW1965050184

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.