FAM 83G/Fam83g genetic variants affect canine and murine hair formation-Reference-Cited by-同舟云学术

FAM 83G/Fam83g genetic variants affect canine and murine hair formation

Published:2018-08-03 Issue:4 Volume:28 Page:350-354
ISSN:0906-6705
Container-title:Experimental Dermatology
language:en
Short-container-title:Exp Dermatol

Author:

Balmer Pierre¹²,Fellay Auxanne K.¹,Sayar Beyza S.²³,Hariton William V. J.²³,Wiener Dominique J.²⁴,Galichet Arnaud²³⁵,Müller Eliane J.²³⁴⁵,Roosje Petra J.¹²^ORCID

Affiliation:

1. Division of Clinical DermatologyDepartment of Clinical Veterinary MedicineVetsuisse FacultyUniversity of Bern Bern Switzerland

2. Dermfocus, Vetsuisse FacultyUniversity of Bern Bern Switzerland

3. Department of Clinical ResearchMolecular Dermatology and Stem Cell ResearchUniversity of Bern Bern Switzerland

4. Institute of Animal PathologyVetsuisse FacultyUniversity of Bern Bern Switzerland

5. Clinic for DermatologyInselspitalBern University Hospital Bern Switzerland

Publisher

Wiley

Subject

Dermatology,Molecular Biology,Biochemistry

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1111/exd.13729

Reference17 articles.

1. A Mutation in the FAM83G Gene in Dogs with Hereditary Footpad Hyperkeratosis (HFH)

2. The wooly mutation (wly) on mouse chromosome 11 is associated with a genetic defect in Fam83g

3. 180 Mutations in FAM83G/PAWS1 cause autosomal recessive palmoplantar keratoderma with leukonychia and abundant curly hair

4. Protein associated with SMAD1 (PAWS1/FAM83G) is a substrate for type I bone morphogenetic protein receptors and modulates bone morphogenetic protein signalling

5. Analyses of regenerative wave patterns in adult hair follicle populations reveal macro-environmental regulation of stem cell activity

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5. Pathogenic FAM83G palmoplantar keratoderma mutations inhibit the PAWS1:CK1α association and attenuate Wnt signalling.;Wellcome Open Research;2020-02-17