Variability in dentofacial phenotypes in four families with WNT10A mutations

[1]  P. Jagodziński,et al.  Nucleotide variants of genes encoding components of the Wnt signalling pathway and the risk of non‐syndromic tooth agenesis , 2013, Clinical genetics.

[2]  P. Calvas,et al.  Mutations in WNT10A are frequently involved in oligodontia associated with minor signs of ectodermal dysplasia , 2013, American journal of medical genetics. Part A.

[3]  D. Lindhout,et al.  Mutations in WNT10A are present in more than half of isolated hypodontia cases , 2012, Journal of Medical Genetics.

[4]  O. MacDougald,et al.  Wnt6, Wnt10a and Wnt10b inhibit adipogenesis and stimulate osteoblastogenesis through a β-catenin-dependent mechanism. , 2012, Bone.

[5]  G. Petrof,et al.  Schöpf–Schulz–Passarge syndrome resulting from a homozygous nonsense mutation, p.Cys107X, in WNT10A , 2011, The Australasian journal of dermatology.

[6]  W. Ahmad,et al.  Two novel mutations in the gene EDAR causing autosomal recessive hypohidrotic ectodermal dysplasia. , 2011, Orthodontics & craniofacial research.

[7]  N. Dahl,et al.  Isolated oligodontia associated with mutations in EDARADD, AXIN2, MSX1, and PAX9 genes , 2011, American journal of medical genetics. Part A.

[8]  P. Kantaputra,et al.  WNT10A and isolated hypodontia , 2011, American journal of medical genetics. Part A.

[9]  J. McGrath,et al.  Intra-familial variability of ectodermal defects associated with WNT10A mutations. , 2011, Acta dermato-venereologica.

[10]  S. Heath,et al.  Two families confirm Schöpf‐Schulz‐Passarge syndrome as a discrete entity within the WNT10A phenotypic spectrum , 2011, Clinical genetics.

[11]  A. Smahi,et al.  Only four genes (EDA1, EDAR, EDARADD, and WNT10A) account for 90% of hypohidrotic/anhidrotic ectodermal dysplasia cases , 2011, Human mutation.

[12]  D. Murrell,et al.  Phenotypic variability associated with WNT10A nonsense mutations , 2010, The British journal of dermatology.

[13]  J. McGrath,et al.  Schöpf-Schulz-Passarge syndrome resulting from a homozygous nonsense mutation in WNT10A. , 2010, Journal of dermatological science.

[14]  Steven P. Jones,et al.  A cephalometric study to investigate the skeletal relationships in patients with increasing severity of hypodontia. , 2010, The Angle orthodontist.

[15]  Boris Jerchow,et al.  Reciprocal requirements for EDA/EDAR/NF-kappaB and Wnt/beta-catenin signaling pathways in hair follicle induction. , 2009, Developmental cell.

[16]  S. Sel,et al.  WNT10A mutations are a frequent cause of a broad spectrum of ectodermal dysplasias with sex-biased manifestation pattern in heterozygotes. , 2009, American journal of human genetics.

[17]  P. Nieminen.  Genetic basis of tooth agenesis. , 2009, Journal of experimental zoology. Part B, Molecular and developmental evolution.

[18]  S. Baig,et al.  WNT10A missense mutation associated with a complete Odonto-Onycho-Dermal Dysplasia syndrome , 2009, European Journal of Human Genetics.

[19]  P. D. De Coster,et al.  Dental agenesis: genetic and clinical perspectives. , 2008, Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology.

[20]  E. Chouery,et al.  Mutation in WNT10A is associated with an autosomal recessive ectodermal dysplasia: the odonto-onycho-dermal dysplasia. , 2007, American journal of human genetics.

[21]  T. Yamashiro,et al.  Wnt10a regulates dentin sialophosphoprotein mRNA expression and possibly links odontoblast differentiation and tooth morphogenesis. , 2007, Differentiation; research in biological diversity.

[22]  P. Krieg,et al.  Census of vertebrate Wnt genes: Isolation and developmental expression of Xenopus Wnt2, Wnt3, Wnt9a, Wnt9b, Wnt10a, and Wnt16 , 2007, Developmental dynamics : an official publication of the American Association of Anatomists.

[23]  Anne Marie Kuijpers-Jagtman,et al.  A meta-analysis of the prevalence of dental agenesis of permanent teeth. , 2004 .

[24]  I. Thesleff,et al.  Mutations in AXIN2 cause familial tooth agenesis and predispose to colorectal cancer. , 2004, American journal of human genetics.

[25]  K. Kratochwil,et al.  FGF4, a direct target of LEF1 and Wnt signaling, can rescue the arrest of tooth organogenesis in Lef1(-/-) mice. , 2002, Genes & development.

[26]  S. Millar,et al.  WNT signals are required for the initiation of hair follicle development. , 2002, Developmental cell.

[27]  J. Seidman,et al.  A nonsense mutation in MSX1 causes Witkop syndrome. , 2001, American journal of human genetics.

[28]  J. Kere,et al.  Ectodysplasin is released by proteolytic shedding and binds to the EDAR protein. , 2001, Human molecular genetics.

[29]  T. Starink.  Eccrine syringofibroadenoma: multiple lesions representing a new cutaneous marker of the Schöpf syndrome, and solitary nonhereditary tumors. , 1997, Journal of the American Academy of Dermatology.

[30]  D. Schlessinger,et al.  X–linked anhidrotic (hypohidrotic) ectodermal dysplasia is caused by mutation in a novel transmembrane protein , 1996, Nature Genetics.

[31]  H. S. Duterloo,et al.  Development of the human dentition: An atlas , 1976 .