Wnt family member 10A
עודכן לאחרונה 18 Aug 2020
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ה WNT10A gene is part of a large family of WNT genes, which play critical roles in development starting before birth. These genes provide instructions for making proteins that participate in chemical signaling pathways in the body. Wnt signaling controls the activity of certain genes and regulates the interactions between cells during embryonic development.
Normal function
ה WNT10A gene is part of a large family of WNT genes, which play critical roles in development starting before birth. These genes provide instructions for making proteins that participate in chemical signaling pathways in the body. Wnt signaling controls the activity of certain genes and regulates the interactions between cells during embryonic development.
The protein produced from the WNT10A gene plays a role in the development of many parts of the body. It appears to be essential for the formation of tissues that arise from an embryonic cell layer called the ectoderm. These tissues include the skin, hair, nails, teeth, and sweat glands. Researchers believe that the WNT10A protein is particularly important for the formation and shaping of both baby (primary) teeth and adult (permanent) teeth.
Conditions referring to this gene or chromosome
Other names
OODD
protein Wnt-10a precursor
STHAG4
wingless-type MMTV integration site family, member 10A
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קריאה נוספת והפניות
- Wnt family member 10A; MedlinePlus, National Library of Medicine.
- Adaimy L, Chouery E, Megarbane H, Mroueh S, Delague V, Nicolas E, Belguith H, de Mazancourt P, Megarbane A. Mutation in WNT10A is associated with an autosomal recessive ectodermal dysplasia: the odonto-onycho-dermal dysplasia. Am J Hum Genet. 2007 Oct;81(4):821-8. doi: 10.1086/520064. Epub 2007 Aug 9.
- Arzoo PS, Klar J, Bergendal B, Norderyd J, Dahl N. WNT10A mutations account for (1/4) of population-based isolated oligodontia and show phenotypic correlations. Am J Med Genet A. 2014 Feb;164A(2):353-9. doi: 10.1002/ajmg.a.36243. Epub 2013 Nov 25.
- Bohring A, Stamm T, Spaich C, Haase C, Spree K, Hehr U, Hoffmann M, Ledig S, Sel S, Wieacker P, Ropke A. WNT10A mutations are a frequent cause of a broad spectrum of ectodermal dysplasias with sex-biased manifestation pattern in heterozygotes. Am J Hum Genet. 2009 Jul;85(1):97-105. doi: 10.1016/j.ajhg.2009.06.001. Epub 2009 Jun 25.
- Cluzeau C, Hadj-Rabia S, Jambou M, Mansour S, Guigue P, Masmoudi S, Bal E, Chassaing N, Vincent MC, Viot G, Clauss F, Maniere MC, Toupenay S, Le Merrer M, Lyonnet S, Cormier-Daire V, Amiel J, Faivre L, de Prost Y, Munnich A, Bonnefont JP, Bodemer C, Smahi A. Only four genes (EDA1, EDAR, EDARADD, and WNT10A) account for 90% of hypohidrotic/anhidrotic ectodermal dysplasia cases. Hum Mutat. 2011 Jan;32(1):70-2. doi: 10.1002/humu.21384.
- Kantaputra P, Kaewgahya M, Jotikasthira D, Kantaputra W. Tricho-odonto-onycho-dermal dysplasia and WNT10A mutations. Am J Med Genet A. 2014 Apr;164A(4):1041-8. doi: 10.1002/ajmg.a.36388. Epub 2014 Jan 23.
- Mues G, Bonds J, Xiang L, Vieira AR, Seymen F, Klein O, D'Souza RN. The WNT10A gene in ectodermal dysplasias and selective tooth agenesis. Am J Med Genet A. 2014 Oct;164A(10):2455-60. doi: 10.1002/ajmg.a.36520. Epub 2014 Apr 3.
- Plaisancie J, Bailleul-Forestier I, Gaston V, Vaysse F, Lacombe D, Holder-Espinasse M, Abramowicz M, Coubes C, Plessis G, Faivre L, Demeer B, Vincent-Delorme C, Dollfus H, Sigaudy S, Guillen-Navarro E, Verloes A, Jonveaux P, Martin-Coignard D, Colin E, Bieth E, Calvas P, Chassaing N. Mutations in WNT10A are frequently involved in oligodontia associated with minor signs of ectodermal dysplasia. Am J Med Genet A. 2013 Apr;161A(4):671-8. doi: 10.1002/ajmg.a.35747. Epub 2013 Feb 7.
- Tardieu C, Jung S, Niederreither K, Prasad M, Hadj-Rabia S, Philip N, Mallet A, Consolino E, Sfeir E, Noueiri B, Chassaing N, Dollfus H, Maniere MC, Bloch-Zupan A, Clauss F. Dental and extra-oral clinical features in 41 patients with WNT10A gene mutations: A multicentric genotype-phenotype study. Clin Genet. 2017 Nov;92(5):477-486. doi: 10.1111/cge.12972. Epub 2017 Mar 19.
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