Evidence map›Paper›PMID 18572160›Full record

ArticleDevelopmental biology2008

TGF-beta type I receptor Alk5 regulates tooth initiation and mandible patterning in a type II receptor-independent manner.

Hu Zhao, Kyoko Oka, Pablo Bringas, Vesa Kaartinen, Yang Chai

Abstract read
In one paragraph

Article in Developmental biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

46 citing papers in PubMed, 69 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Assessing candidate DLX-regulated genes in the first pharyngeal arch of chick embryos.Developmental dynamics : an official publication of the American Association of Anatomists · 2025
    Article
  6. A Chemically Defined Culture for Tooth Reconstitution.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Bone or Tooth dentin: The TGF-β signaling is the key.International journal of biological sciences · 2024
    Article
  11. Article
  12. Tooth number abnormality: from bench to bedside.International journal of oral science · 2023
    Review
  13. Article
  14. Review
  15. Article
  16. Frontiers in cell and developmental biology · 2022
    Article
  17. Article
  18. Review
  19. Article
  20. Article
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

5 authors at 2 institutions in 1 country.

Hu ZhaoCenter for Craniofacial Molecular Biology, School of Dentistry, University of Southern California, 2250 Alcazar Street, CSA 103, Los Angeles, CA 90033, USA.
Kyoko Oka
Pablo Bringas
Vesa Kaartinen
Yang Chai
University of Southern California · USChildren's Hospital of Los Angeles · US

Funding

TGF BETA SIGNALING AND MANDIBULAR MORPHOGENESISR01DE012711 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHAI, YANG · 1999 to 2023
$5.7M
TGF BETA SIGNALING AND CRANIOFACIAL MORPHOGENESISR37DE012711 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHAI, YANG · 2009 to 2018
$4.3M
MOLECULAR REGULATORY MECHANISM OF TONGUE MORPHOGENESISR01DE014078 · NIDCR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHAI, YANG · 2003 to 2013
$3.4M
NIDCR NIH HHS DE012711NIDCR NIH HHS DE014078NIDCR NIH HHS R01 DE012711NIDCR NIH HHS R01 DE014078NIDCR NIH HHS R37 DE012711
6 · The paper itself

Abstract

TGF-beta superfamily members signal through a heteromeric receptor complex to regulate craniofacial development. TGF-beta type II receptor appears to bind only TGF-beta, whereas TGF-beta type I receptor (ALK5) also binds to ligands in addition to TGF-beta. Our previous work has shown that conditional inactivation of Tgfbr2 in the neural crest cells of mice leads to severe craniofacial bone defects. In this study, we examine and compare the defects of TGF-beta type II receptor (Wnt1-Cre;Tgfbr2(fl/fl)) and TGF-beta type I receptor/Alk5 (Wnt1-Cre;Alk5(fl)(/fl)) conditional knockout mice. Loss of Alk5 in the neural crest tissue resulted in phenotypes not seen in the Tgfbr2 mutant, including delayed tooth initiation and development, defects in early mandible patterning and altered expression of key patterning genes including Msx1, Bmp4, Bmp2, Pax9, Alx4, Lhx6/7 and Gsc. Alk5 controls the survival of CNC cells by regulating expression of Gsc and other genes in the proximal aboral region of the developing mandible. We conclude that ALK5 regulates tooth initiation and early mandible patterning through a pathway independent of Tgfbr2. There is an intrinsic requirement for Alk5 signal in regulating the fate of CNC cells during tooth and mandible development.

Indexed as

Body PatterningAnimalsApoptosisCell DifferentiationDental EnamelEmbryo, MammalianGene DeletionGene Expression Regulation, DevelopmentalHedgehog ProteinsIntegrasesLymphoid Enhancer-Binding Factor 1MandibleMiceMice, KnockoutModels, BiologicalMutationCre recombinaseHedgehog ProteinsIntegrasesLef1 protein, mouseLymphoid Enhancer-Binding Factor 1Protein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IIShh protein, mouseTgfbr1 protein, mouseWnt Proteins

Identifiers

PMID18572160
PMCPMC3629921
OpenAlexW1979892487

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.