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Deficiency of 14-3-3ε and 14-3-3ζ by the Wnt1 promoter-driven Cre recombinase results in pigmentation defects
Journal article   Open access   Peer reviewed

Deficiency of 14-3-3ε and 14-3-3ζ by the Wnt1 promoter-driven Cre recombinase results in pigmentation defects

Brett Cornell and Kazuhito Toyo-oka
BMC research notes, v 9(1), pp 180-180
22 Mar 2016
DOI: https://doi.org/10.1186/s13104-016-1980-z
PMID: 27001213
url
https://bmcresnotes.biomedcentral.com/track/pdf/10.1186/s13104-016-1980-zView
Published, Version of Record (VoR) Open
url
https://doi.org/10.1186/s13104-016-1980-zView
Published, Version of Record (VoR) Open

Abstract

14-3-3 Proteins - deficiency 14-3-3 Proteins - metabolism Animals Body Weight Craniofacial Abnormalities - pathology Crosses, Genetic Female Integrases - metabolism Male Mice Neural Crest - metabolism Pigmentation - genetics Promoter Regions, Genetic Wnt1 Protein - metabolism
The seven 14-3-3 protein isoforms bind to numerous proteins and are involved in a wide variety of cellular events, including the cell cycle, cell division, apoptosis and cancer. We previously found the importance of 14-3-3 proteins in neuronal migration of pyramidal neurons in the developing cortex. Here, we test the function of 14-3-3 proteins in the development of neural crest cells in vivo using mouse genetic approaches. We found that 14-3-3 proteins are important for the development of neural crest cells, in particular for the pigmentation of the fur on the ventral region of mice. Our data obtained from the 14-3-3ε/14-3-3ζ/Wnt1-Cre mice strongly indicate the importance of 14-3-3 proteins in the development of melanocyte lineages.

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