Wnt signaling in orofacial clefts: crosstalk, pathogenesis and models-Reference-Cited by-同舟云学术

Wnt signaling in orofacial clefts: crosstalk, pathogenesis and models

Published:2019-02-01 Issue:2 Volume:12 Page:
ISSN:1754-8411
Container-title:Disease Models & Mechanisms
language:en
Short-container-title:

Author:

Reynolds Kurt¹²³,Kumari Priyanka¹²,Sepulveda Rincon Lessly¹²,Gu Ran¹²,Ji Yu¹²³,Kumar Santosh¹²,Zhou Chengji J.¹²³^ORCID

Affiliation:

1. Department of Biochemistry and Molecular Medicine, University of California at Davis, School of Medicine, Sacramento, CA 95817, USA

2. Institute for Pediatric Regenerative Medicine of Shriners Hospitals for Children, University of California at Davis, School of Medicine, Sacramento, CA 95817, USA

3. Biochemistry, Molecular, Cellular, and Developmental Biology (BMCDB) Graduate Group, University of California, Davis, CA 95616, USA

Abstract

ABSTRACT Diverse signaling cues and attendant proteins work together during organogenesis, including craniofacial development. Lip and palate formation starts as early as the fourth week of gestation in humans or embryonic day 9.5 in mice. Disruptions in these early events may cause serious consequences, such as orofacial clefts, mainly cleft lip and/or cleft palate. Morphogenetic Wnt signaling, along with other signaling pathways and transcription regulation mechanisms, plays crucial roles during embryonic development, yet the signaling mechanisms and interactions in lip and palate formation and fusion remain poorly understood. Various Wnt signaling and related genes have been associated with orofacial clefts. This Review discusses the role of Wnt signaling and its crosstalk with cell adhesion molecules, transcription factors, epigenetic regulators and other morphogenetic signaling pathways, including the Bmp, Fgf, Tgfβ, Shh and retinoic acid pathways, in orofacial clefts in humans and animal models, which may provide a better understanding of these disorders and could be applied towards prevention and treatments.

Funder

National Institutes of Health

Shriners Hospitals for Children

Publisher

The Company of Biologists

Subject

General Biochemistry, Genetics and Molecular Biology,Immunology and Microbiology (miscellaneous),Medicine (miscellaneous),Neuroscience (miscellaneous)

Link

http://journals.biologists.com/dmm/article-pdf/doi/10.1242/dmm.037051/1863790/dmm037051.pdf

Reference357 articles.

1. Retinoids and epidermal growth factor alter embryonic mouse palatal epithelial and mesenchymal cell differentiation in organ culture;Abbott;J. Craniofac. Genet. Dev. Biol.,1987

2. Etiology of retinoic acid-induced cleft palate varies with the embryonic stage;Abbott;Teratology,1989

3. Craniofacial development: discoveries made in the chicken embryo;Abramyan;Int. J. Dev. Biol.,2018

4. Recessive Robinow syndrome, allelic to dominant brachydactyly type B, is caused by mutation of ROR2;Afzal;Nat. Genet.,2000

5. The cellular and molecular etiology of the cleft secondary palate in Fgf10 mutant mice;Alappat;Dev. Biol.,2005

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