Evidence map›Paper›PMID 18723525›Full record

ArticleHuman molecular genetics2008

Novel expression and transcriptional regulation of FoxJ1 during oro-facial morphogenesis.

Shankar R Venugopalan, Melanie A Amen, Jianbo Wang, Leeyean Wong, Adriana C Cavender, Rena N D'Souza, Mikael Akerlund, Steve L Brody, Tord A Hjalt, Brad A Amendt

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

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  19. The Pitx2c N-terminal domain is a critical interaction domain required for asymmetric morphogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2009
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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

10 authors at 5 institutions in 2 countries.

Shankar R VenugopalanTexas A&M Health Science Center, Institute of Biosciences and Technology, Houston, TX 77030, USA.
Melanie A Amen
Jianbo Wang
Leeyean Wong
Adriana C Cavender
Rena N D'Souza
Mikael Akerlund
Steve L Brody
Tord A Hjalt
Brad A Amendt
Mitchell Institute · USBaylor College of Medicine · USLund University · SETexas A&M Health Science Center · USWashington University in St. Louis · US

Funding

Pilot--Health Science ResearchP30ES009106 · NIEHS · TEXAS A&M UNIVERSITY SYSTEM · PI SAFE, STEPHEN H. · 1998 to 2006
$9.2M
Molecular Mechanisms of PITX2 During Craniofacial DevelopmentR01DE013941 · NIDCR · UNIVERSITY OF TULSA · PI AMENDT, BRAD A · 2000 to 2013
$4.2M
NIDCR NIH HHS DE 13941NIDCR NIH HHS R01 DE013941NIEHS NIH HHS ES09106NIEHS NIH HHS P30 ES009106
6 · The paper itself

Abstract

Axenfeld-Rieger syndrome (ARS) patients with PITX2 point mutations exhibit a wide range of clinical features including mild craniofacial dysmorphism and dental anomalies. Identifying new PITX2 targets and transcriptional mechanisms are important to understand the molecular basis of these anomalies. Chromatin immunoprecipitation assays demonstrate PITX2 binding to the FoxJ1 promoter and PITX2C transgenic mouse fibroblasts and PITX2-transfected cells have increased endogenous FoxJ1 expression. FoxJ1 is expressed at embryonic day 14.5 (E14.5) in early tooth germs, then down-regulated from E15.5-E17.5 and re-expressed in the inner enamel epithelium, oral epithelium, tongue epithelium, sub-mandibular salivary gland and hair follicles during E18.5 and neonate day 1. FoxJ1 and Pitx2 exhibit overlapping expression patterns in the dental and oral epithelium. PITX2 activates the FoxJ1 promoter and, Lef-1 and beta-catenin interact with PITX2 to synergistically regulate the FoxJ1 promoter. FoxJ1 physically interacts with the PITX2 homeodomain to synergistically regulate FoxJ1, providing a positive feedback mechanism for FoxJ1 expression. Furthermore, FoxJ1, PITX2, Lef-1 and beta-catenin act in concert to activate the FoxJ1 promoter. The PITX2 T68P ARS mutant protein physically interacts with FoxJ1; however, it cannot activate the FoxJ1 promoter. These data indicate a mechanism for the activity of the ARS mutant proteins in specific cell types and provides a basis for craniofacial/ tooth anomalies observed in these patients. These data reveal novel transcriptional mechanisms of FoxJ1 and demonstrate a new role of FoxJ1 in oro-facial morphogenesis.

Indexed as

Gene Expression Regulation, DevelopmentalMaxillofacial DevelopmentMorphogenesisTranscription, GeneticAnimalsCHO CellsCraniofacial AbnormalitiesCricetinaeCricetulusFaceFemaleForkhead Transcription FactorsHomeobox Protein PITX2Homeodomain ProteinsHumansMaleForkhead Transcription FactorsFOXJ1 protein, humanHomeobox Protein PITX2Homeodomain ProteinsTranscription Factors

Identifiers

PMID18723525
PMCPMC2733810
OpenAlexW2133834926

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.